Judith White, MD, PhD
DESCRIPTION 
Dizziness is a common, nonspecific term used to describe a range of sensations including the illusion of movement of the visual surround (vertigo), lightheadedness, near-syncope, or postural instability. The etiology may be central or peripheral, with a broad differential, ranging from benign to life-threatening conditions. Vertigo is predictive of involvement of the vestibular system (peripheral or central). The historical characteristics and duration of symptoms, and any provoking or alleviating factors, are helpful in narrowing the diagnosis.
- Clinical characteristics
- Dizziness can affect patients of all ages; however, it is more common in elderly patients. It is one of the most common diagnoses for which adults seek medical evaluation, affecting 15–30% of the population at some point during their lifetime. There is a slight female preponderance. All races are affected equally.
- Risk factors for dizziness include older age, diabetes, infections, inner ear problems, vision problems, trauma, hypertension, dehydration, orthostatic hypotension, atherosclerotic vascular disease, anemia, menopause, and familial factors.
PATHOPHYSIOLOGY
- The vestibular labyrinth contains the semicircular canals and the otolithic organs (saccule and utricle). Neural discharge rates vary depending on linear and angular acceleration, and innervate the vestibular nuclei and central vestibulo-ocular and vestibulo-spinal pathways. Acute loss of unilateral vestibular function produces the acute vestibular syndrome, characterized by nausea and vomiting, vertigo, nystagmus, and postural instability. Symptoms usually persist for days and gradually subside over weeks.
- Acute vestibular syndrome is usually peripheral in origin, but central pathology such as infarction and hemorrhage of the inferior cerebellum may simulate peripheral symptoms in up to 25% of patients in emergency settings with central risk factors (age over 65, diabetes, hypertension, smoking, and heart or atherosclerotic disease). Some who present with isolated acute vestibular syndrome have infarction of the inferior cerebellum. Severe imbalance is a finding which predicts central pathology in this group.
[Outline]
The characteristics of the dizzy sensation (vertigo vs. pre-syncope, imbalance, or lightheadedness) are helpful to narrow diagnostic categories. In patients with vertigo, the duration is especially helpful in diagnosis. Vertigo lasting for seconds, occurring with position change, suggests benign paroxysmal positional vertigo. Vertigo lasting for hours associated with hearing change, tinnitus, and fullness suggests Meniere's syndrome. Acute onset of vertigo lasting for days to weeks suggests acute vestibular syndrome. Episodic vertigo in a patient without other features, with a history of migraine, is commonly migraine associated. Vertigo associated with loud sounds or pressure changes may be seen in dehiscence of the vertical semicircular canals. Imbalance without vertigo is seen in bilateral vestibular hypofunction.
DIAGNOSTIC TESTS AND INTERPRETATION
Lab
Blood tests have a low yield in identifying a specific cause of dizziness.
Diagnostic Procedures/Other
Positioning testing including the Dix–Hallpike can be helpful to distinguish peripheral causes of dizziness, such as benign paroxysmal positional vertigo, and may be performed in the emergency department without special equipment. Examination with Frenzel lenses or eliminating visual fixation in low room light or placing a uniform blank surface in front of the patient's eyes can reveal nystagmus. Formal laboratory tests of audio-vestibular function may be of benefit in challenging cases, including audiometry, electronystagmography, and rotational testing.
Imaging
MRI, with and without contrast, is important to exclude structural lesions or malformations of the soft tissue, such as acoustic neuroma, infarction, or demyelinating disorders. CT scan of the temporal bones, without contrast, with fine cuts, and reconstruction in the plane of the semicircular canals, is helpful in identifying semicircular canal dehiscence. Imaging studies are strongly indicated for patients with focal neurological findings, marked imbalance, or persistent unexplained dizziness. MR and cerebral angiography are used to identify vertebrobasilar insufficiency or atherosclerosis.
DIFFERENTIAL DIAGNOSIS
- Benign paroxysmal positional vertigo
- Superior semicircular canal dehiscence
- Vestibular neuronitis
- Ramsay Hunt syndrome
- Meniere's syndrome
- Multiple sclerosis
- Migraine-associated dizziness
- Autonomic dysfunction
- Orthostatic hypotension
- Hypoglycemia
- Infections (otitis media, syphilis, meningitis, AIDS, viral encephalitis)
- CNS vasculitis
- Cerebellar lesion (infarct, vascular malformation, hemorrhage, neoplasm)
- Lateral medullary syndrome
- Pontine syndrome
- Posterior fossa neoplasm (e.g., acoustic neuroma, brainstem glioma)
- Neurofibromatosis type 2
- Paraneoplastic syndrome
- Posterior fossa structural lesion (e.g., Chiari malformation)
- Postconcussion syndrome
- Alcoholic cerebellar degeneration
- Vitamin E deficiency
- Vitamin B12 or folate deficiency
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MEDICATION
- Vestibular suppressants are useful for brief (3 days or less) control of symptoms associated with acute vestibular syndrome. They are not indicated for long-term management of dizziness, and have no proven effect in benign paroxysmal positional vertigo.
- Antihistamines: Meclizine (Antivert 25–50 mg q6h PRN PO) is most commonly used; dimenhydrinate (Dramamine 50 mg q4–6h PO or IM) is also used as a vestibular sedative medication. Central anticholinergic activity may be the underlying mechanism.
- Benzodiazepines: Diazepam (Valium 2.5–5 mg t.i.d. or PRN PO, IM, or IV) or clonazepam (Klonopin 0.5 mg t.i.d. PO) can be helpful in alleviating severe vertigo and anxiety. Care should be taken to avoid tolerance and habituation.
- Anticholinergics: Scopolamine transdermal patch is effective for motion sickness and posttraumatic vertigo.
- Antiemetics
- Promethazine (Phenergan, 25 mg q6h PRN by mouth, or via suppository) and prochlorperazine (Compazine 5–10 mg q6h PO or IM, or 25 mg q12h suppository) are useful in relieving the severe nausea associated with vertigo. Ondansetron (4 mg q8h PRN) and prochlorperazine are used for severe nausea from central vertigo.
- For Meniere's disease, 1,500 mg/day low-sodium diet and diuretics (triamterene/hydrochlorothiazide 37.5/25 once a day by mouth) are helpful. Intratympanic steroids are useful if episodic vertigo persists. Rarely, chemical labyrinthectomy with intratympanic gentamicin is indicated.
- For acute vestibular neuritis, prednisone 1 mg/kg/day for 10 days has been suggested to improve recovery.
- Contraindications: Prior history of hypersensitivity or allergic reaction. Transtympanic aminoglycoside treatment of Meniere's disease is associated with risk of profound hearing loss; bilateral involvement of Meniere's disease is a relative contraindication for ototoxic treatment.
- Precautions: Drowsiness is commonly associated with antihistamines and antiemetics. Steroid therapy for vestibular neuritis can be associated with hypertension, psychiatric symptoms, hyperglycemia, gastric ulcers, osteoporosis, hip necrosis, and cataract.
ADDITIONAL TREATMENT
General Measures
Specific therapies are directed to the underlying etiology of the dizziness. Canalith repositioning is highly effective in benign paroxysmal positional vertigo. Vestibular exercises and rehabilitation programs are designed to readjust perceptual, vestibulo-ocular, and vestibulo-spinal reflexes by fostering central compensation of vestibular tone imbalance, and minimizing fall risk.
COMPLEMENTARY AND ALTERNATIVE THERAPIES
- Symptomatic treatment
- Adjunctive treatments
- In the acute phase, bed rest, adequate hydration, mental relaxation, and visual fixation are helpful. Vestibular habituation and balance retraining exercises are beneficial for chronic persistent dizziness secondary to multiple sensory deficits. Physical and occupational therapies involving eye, head, and body movements are also beneficial for dizziness due to upper cervical dysfunction and cerebrovascular accident, and should be begun as soon as the acute stage of nausea and vomiting has ended.
SURGERY/OTHER PROCEDURES
In patients with refractory Meniere's syndrome, surgical intervention such as endolymphatic shunt placement and selective vestibular nerve section can be performed, although intratympanic therapies are commonly attempted prior to invasive surgical therapies. Semicircular canal dehiscence may be treated with canal occlusion.
IN-PATIENT CONSIDERATIONS
Admission Criteria
Patients with profound disequilibrium or intractable vomiting may require imaging studies, hospitalization, and IV rehydration. The presence of focal neurological findings other than nystagmus warrants thorough evaluation of possible central pathology.
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FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
Patients are followed to monitor progression and recurrence of symptoms and efficacy of pharmacologic and rehabilitation therapy. This can be done with serial physical exams and specific outcome measures such as the Dizziness Handicap Inventory, Activities Specific Balance Confidence Scale, Computerized Dynamic Posturography, and gait measures.
PATIENT EDUCATION
- Vestibular Disorders Association, P.O. Box 4467, Portland, OR 97208-4467. Website: www.vestibular.org
- Balance and Dizziness Disorders Society in Canada, 5525 West Boulevard, #325, Vancouver, BC, Canada V6M 3W6. Website: www.BalanceAndDizziness.org
- Meniere's Society, 98 Maybury Rd., Working Surrey, GU21 5HX, UK
PROGNOSIS
Clinical course and prognosis varies with etiology. Most cases of dizziness are benign and self-limited, and recover spontaneously over several weeks to months. Symptomatic recovery is due to vestibular compensation (central reorganization of vestibular circuits). Prognosis is better if the symptoms are due to vestibular dysfunction. In dizziness of central origin or from systemic illness, success depends on treating the underlying disorder.
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