Dizziness, Vertigo, and Imbalance Treatment & Management

Acute dizziness and vertigo is usually managed with vestibular suppressants, antiviral medication, and antiemetic medications. Steroids are useful in selected patients. Vestibular suppressants should be used for a few days at most because they delay the brain’s natural compensatory mechanism for peripheral vertigo. Vestibular rehabilitation is very useful in boosting central vestibular compensation.

Vestibular neuronitis

Vestibular neuronitis is the most common cause of acute vertigo, with an incidence of 170 cases per 100,000 people. It is believed to result from reactivation of herpes simplex virus infection that affects the vestibular ganglion and vestibular nerves. ^[11] A prodromal upper respiratory tract illness may or may not be present. Vertigo is without auditory or other central nervous system (CNS) symptoms and lasts for several days. Patients are usually ill and cannot perform home or work activities. They are commonly rated symptomatically.

A brief course of antiemetic and vestibular suppressants is usually needed in the acute phase but should be withdrawn as soon as possible to facilitate the process of central vestibular compensation. ^[11] Corticosteroids may improve long-term outcomes. Early vestibular rehabilitation is important. ^[11] Antiviral medications have not proved helpful, possibly because a large spectrum of viruses can cause vestibular neuronitis. The pharmacological treatment of choice for acute vestibular neuritis is oral steroids beginning as soon as possible with gradual tapering of the dose. One third of patients have chronic vestibular symptoms and develop benign paroxysmal positioning vertigo (BPPV).

Benign paroxysmal positioning vertigo

BPPV is the second most common cause of vertigo. The typical symptom is brief episodic vertigo upon changing head or body position. Patients may have a residual sensation of disequilibrium between episodes. BPPV is commonly either idiopathic or posttraumatic. Other causes of vertigo, such as vestibular neuronitis, Ménière disease, and delayed endolymphatic hydrops, are also associated with BPPV.

The mechanism of BPPV can involve canalithiasis (otoconia floating in the endolymph) or cupulolithiasis (otoconia adherent to cupula). The most commonly affected canal is the posterior canal (90% of cases); the horizontal canal may also be affected, but to a lesser extent.

The American Academy of Neurology has published a practice parameter for the treatment of BPPV. ^[12] The most effective treatment is canalith repositioning from the affected canal back to the vestibule where it is absorbed using the most common maneuvers: Epley, Semont, Lempert, and Hamid (for horizontal canal cupulolithiasis). Medications can be helpful for short-term reduction of symptoms but have not been shown to be effective in the long-term treatment of BPPV.

It is important to note that most cases of BPPV can be treated in the office once the history and examination confirm the diagnosis. Prolonged sessions of physical therapy are not necessary and not cost effective. Some of these patients may also require medications, which should be given under physician supervision, to treat severe nausea and vomiting that can result from CRP treatments.

The most common complication of the Semont or Epley maneuver is conversion of the posterior canal−horizontal canal BPPV, which is treated with the Lempert or Hamid maneuvers. A less common complication is undue cervical strain, which is especially likely with the Semont maneuver or with neck hyperextension during the Epley maneuver.

Ménière disease

Ménière disease is a disorder of the inner ear with typical symptoms of episodic vertigo, tinnitus, and hearing loss. Untreated, severe hearing loss and unilateral vestibular paresis are inevitable. Bilateral involvement occurs in about 25% of patients. The etiology is idiopathic in most cases and can also be hereditary, autoimmune, infectious, or allergic. The common pathophysiology is disordered fluid homeostasis in the inner ear, with endolymphatic hydrops representing a histologic footprint rather than an etiology.

Most patients respond to conservative therapy with salt restriction and diuretics. Corticosteroids, given orally or intratympanically, can be used to stabilize active disease and to recover speech discrimination, especially when used in early stages of the disease. Intratympanic gentamicin (chemical labyrinthectomy) is a minimally invasive procedure that has emerged as an effective method for treating the disabling vertigo of Ménière disease when hearing loss and speech discrimination have progressed to severe levels. Gentamicin is also very effective in treating Tumarkin attacks of Ménière disease.

The role of surgical therapy for Ménière disease (eg, shunting the endolymphatic sac) is controversial. The literature demonstrates wide variation in the effectiveness, or lack thereof, of surgery.

Autoimmune inner-ear disease

Patients with autoimmune inner-ear disease typically present with rapidly progressive, bilateral hearing loss, with or without vertigo. Initial onset may be unilateral. However, the rapid progression, bilateral involvement, and response to steroids distinguish this disorder from Ménière disease. Autoimmune inner-ear disease can occur with or without other autoimmune disease or laboratory evidence of a systemic inflammatory disorder. Specific laboratory markers for inner-ear antigenicity have low sensitivity and thus are of little clinical utility.

Oral and intratympanic corticosteroids are effective in controlling this disease. Patients with recurrent symptoms that are steroid responsive may benefit from methotrexate or other steroid-sparing medications. These patients should be treated by a rheumatologist.

Migraine

Migraine is a common disorder, affecting 10% of men and 30% of women. About 25% of migraineurs have motion intolerance or sickness rather than true vertigo. The pathophysiology of migraine-associated vestibulopathy is not completely understood. ^[13] Vestibular symptoms usually are dissociated from headaches but sometimes can occur as an aura or as part of a headache. Patients can also have mild form of hearing loss mimicking Ménière disease.

Symptoms that qualify for a diagnosis of vestibular migraine include various types of vertigo and head motion–induced dizziness with nausea. Symptoms must be of moderate or severe intensity. Duration of acute episodes is limited to a window of between 5 minutes and 72 hours. ^[14] Electro/videonystagmography is typically not helpful in differentiating migraine-associated vertigo from other vestibular pathologies. However, for patients with a longstanding history of dizziness, normal findings on electro/videonystagmography are suggestive of migraine-associated dizziness.

For vestibular migraine, the theory of an ion-channel disorder is particularly interesting because different mutations of the CACNA1A gene coding for a transmembrane component of a neuronal calcium channel can provoke familial hemiplegic migraine or episodic ataxia type. ^[15] However, several candidate genes coding for ion-channel proteins have not been found in a population with vestibular migraine. ^[16]

Treatment of migraine-associated vestibulopathy is the same as that of migraine, focusing on adequate control of the frequency and intensity of symptoms using both abortive and prophylactic medications. Triggers should be minimized/eliminated, including disturbed sleep pattern, diet, and lifestyle. ^[13] Prophylactic and abortive medications commonly used in treating migraine should be individually tailored. In the authors’ experience, topiramate and rizatriptan benzoate are associated with long-term control of vestibular migraine.

Transient ischemic attacks

Transient ischemic attacks (TIAs) are episodes of focal neurologic symptoms involving isolated or combined brainstem symptoms such as dizziness, diplopia, or weakness. These attacks are of sudden onset and resolve within 24 hours without residual subjective symptoms or objective signs on examination. TIAs are usually due either to reduced blood flow (the hemodynamic theory; eg, cardiac dysrhythmia) or to obstructed blood flow (the embolic theory; eg, plaques from the heart).

TIAs are commonly (75% of cases) due to posterior circulation (vertebrobasilar territory). The differential diagnosis of TIAs includes migraine, partial seizures, hypoglycemia, syncope, and hyperventilation.

Cerebrovascular disease

Stroke is the third most common cause of death or disability in adults. The vertebrobasilar circulation supplies the brainstem, the cerebellum, and the inner-ear auditory and vestibular structures. Infarction of the cerebellar midline can cause acute vertigo without auditory or other neurologic features (eg, isolated vertigo).

This potentially life-threatening event must be differentiated from vestibular neuronitis. A key difference between these 2 entities is that patients experiencing cerebellar strokes are unable to ambulate without support during the acute vertigo phase. About one half of patients have other features of bulbar or long tract involvement, which make the diagnosis of stroke clear.

Evaluation of the patient with stroke is directed at identifying correctable vascular risk factors (eg, hypertension, diabetes, hyperlipidemia, and smoking) and at determining the mechanism of stroke (eg, small-vessel disease, large-vessel disease, cardioembolism, dissection, hypercoagulability, or vacuities). Secondary prophylactic therapy and rehabilitation are individualized. Both hearing loss and vertigo can occur in the setting of stroke due to central injury, peripheral injury, or both.

Multiple sclerosis

Multiple sclerosis is a disorder of recurrent, inflammatory CNS demyelination that is due to underlying autoimmune disease. The onset is usually at age 20-40 years. Episodes begin over hours to a few days and last weeks to months. Typical symptoms include the following:

• Optic neuritis

• Ocular motor dysfunction

• Trigeminal neuralgia

• Sensorimotor deficits

• Myelopathy

• Ataxia

• Bladder dysfunction

Vertigo, at times mimicking vestibular neuronitis, is a presenting symptom in fewer than 10% of patients. Dizziness or vertigo occurs at some point in the course in one third of patients. Few patients present with hearing loss due to brainstem involvement.

The diagnosis of multiple sclerosis requires the presence of dissemination in time and space (ie, different neurologic symptoms at different times). A careful history, a thorough examination, and serial follow-up combined with magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis help establish the diagnosis; the diagnosis should not be based on MRI abnormalities alone. Disease-modifying therapy is available, but it is only modestly effective. The search for improved treatment is ongoing.

Tumors and malformations of posterior fossa

Vestibular schwannoma (acoustic neuroma) is an uncommon lesion (incidence, 1.1 per 100,000) that typically manifests with slowly progressive unilateral hearing loss and tinnitus. Dizziness is not common, because the vestibular system can usually compensate for such gradual unilateral hypofunction. Dizziness can occur as the tumor expands in the cerebellopontine angle and effaces the brainstem and cerebellum. Arachnoid cysts can also occur in the posterior fossa and result in subtle and nonspecific dizziness and auditory symptoms.

In a cross-sectional observational study in patients with small to medium-sized vestibular schwannomas, over 50% of patients reported ongoing dizziness at a mean of 8 years after treatment. All 538 patients had sporadic vestibular schwannomas of less than 3 cm and underwent primary microsurgery, stereotactic radiosurgery, or observation. The treatment modality was not found to influence long-term dizziness handicap. ^[17]

Chiari malformation occurs in a few adults. It is congenital but often does not become symptomatic until age 20-40 years. Occipital headache precipitated by Valsalva maneuvers, coughing, exertion, or changing position is common. Dizziness may occur with the same precipitants.

Once suspected, the diagnosis can be confirmed by means of MRI. Surgical treatment should be considered for patients whose symptoms are more than mild.

Falls

Upright balance and posture control are not a single physiologic function; they include visual, vestibular, and proprioceptive sensory inputs. During ambulation, the CNS must instantly integrate these inputs and execute appropriate motor plans and purposeful output via an adequate musculoskeletal system. This intricate system changes with age and disease-related decline in any of these systems. For example, bilateral vestibular failure is a contributor in one fourth of elderly patients with disequilibrium. Untreated BPPV can be a risk factor for falls.

The most common fall is a simple event in which the patient has tripped but has no ominous underlying peripheral or central disorder. Hazards in the environment (eg, rugs, electrical wires, poor lighting), polypharmacy, and orthopedic factors often contribute to falls. Because of the substantial risk of injury and the resultant decline in independence or quality of life after a fall, a well-directed evaluation is indicated. Orthostatic hypotension due to aging or medications is also a common contributor. Normal pressure hydrocephalus is also a contributing factor to gait abnormalities and falling.

Vestibular rehabilitation is an important management tool in certain vestibular disorders. It has become widely used in current clinical practice, with many reviews; most lack a critical stance while propagating its use with all vestibular disorders, sometimes using all allowed physical therapy allowances, especially for Medicare patients.

In essence, vestibular rehabilitation aims to minimize and ultimately eliminate the central vestibular asymmetry underlying persistent symptoms of imbalance and unsteadiness. It is different from traditional physical therapy of gait and balance disorders arising from biomechanical or central movement disorders such as Parkinson disease or multiple sclerosis. Vestibular rehabilitation can be performed by patients at home using tailored exercises that focus on challenging the main vestibular reflexes (VOR, VSR) and visual interaction with both reflexes.

In a study of patients who presented to the emergency department with benign paroxysmal positional vertigo, vestibular rehabilitation and medication therapy were shown to be equally efficacious. Of 26 patients, 11 received medications and 15 received vestibular rehabilitation. Two hours after treatment, there was no difference between the two groups regarding the symptoms of nausea or dizziness. Both groups reported a high level of satisfaction, and the length of stay in the ED did not differ between the two groups. ^[18]

Patients who have neck or other biomedical problems should have these problems addressed before starting vestibular rehabilitation. Vestibular rehabilitation is useful for most stable (nonfluctuating) peripheral vestibular disorders such as vestibular neuritis and inactive Ménière disease. It is also helpful for chronic motion intolerance from migraine and after successful treatments of BPPV.

Other forms of balance training programs such as tai chi can be also used, as long as patients can safely incorporate them with vestibular rehabilitation. ^[19]