Vertigo

Article Author:
Monica Stanton
Article Editor:
Andrew Freeman
Updated:
10/27/2018 12:31:59 PM
PubMed Link:
Vertigo

Introduction

Vertigo is a common presenting complaint in primary care offices and emergency departments. It is a symptom of vestibular dysfunction and has been described as a sensation of motion, most commonly rotational motion. It is important to differentiate vertiginous symptoms from other forms of dizziness such as lightheadedness which is most often associated with pre-syncope.

Etiology

Vertigo is most often caused by a dysfunction in the vestibular system from a peripheral or central lesion. 

Peripheral etiologies include the more common causes of vertigo such as benign paroxysmal positional vertigo (BPPV) and Meniere’s disease. BPPV results from calcium deposits or debris in the posterior semicircular canal and causes frequent transient episodes of vertigo lasting a few minutes or less. Unlike BPPV, the patient’s with Ménière’s disease often experience tinnitus, hearing loss and aural fullness in addition to vertigo. Symptoms of Meniere’s disease result from an increased volume of endolymph in the semicircular canals. Two additional distinct causes of peripheral vertigo include acute labyrinthitis and vestibular neuritis. Both arise from inflammation often caused by a viral infection. Another viral induced cause of vertigo includes Herpes zoster oticus, also known as Ramsay Hunt syndrome. In Ramsay Hunt syndrome, vertigo results from reactivation of latent varicella zoster virus (VZV) in the geniculate ganglion leading to inflammation of the vestibulocochlear nerve. The facial nerve is often involved as well resulting in facial paralysis. Less common peripheral causes include a cholesteatoma, otosclerosis, and a perilymphatic fistula. Cholesteatomas are cyst-like lesions filled with keratin debris. Cholesteatomas most often involve the middle ear and mastoid. Otosclerosis is characterized by abnormal growth of bone in the middle ear which leads to conductive hearing loss and may affect the cochlea also causing tinnitus and vertigo. A perilymphatic fistula is another less common cause of peripheral vertigo and results from trauma.

Central etiologies of vertigo should always be considered in the differential. Ischemic or hemorrhagic strokes particularly involving the cerebellum or vertebrobasilar system are life-threatening and must be ruled out by history, physical and other diagnostic tests if warranted. Other more serious central causes include tumors, particularly those arising from the cerebellopontine angle. Examples of such tumors include a brainstem glioma, medulloblastoma, and a vestibular schwannoma which can lead to sensorineural hearing loss as well as vertiginous symptoms. Vestibular migraines are a common central cause of vertigo. They are characterized by unilateral headaches associated with other symptoms including nausea, vomiting, photophobia, and phonophobia. Finally, multiple sclerosis has been associated with both central and peripheral causes of vertigo. Centrally, multiple sclerosis can cause vertigo with the development of demyelinating plaques in the vestibular pathways. BPPV is a common peripheral cause of vertigo in patients with multiple sclerosis.

There are other causes that can lead to vertigo. These include medication-induced vertigo and psychologic disorders including mood, anxiety, and somatization. Medications that have been associated with vertigo include anticonvulsants such as phenytoin and salicylates.

Epidemiology

Vertigo affects both men and women but is about two-thirds more common in women than men. It has been associated with various comorbid conditions including depression and cardiovascular disease. Prevalence increases with age and varies depending on the underlying diagnosis. Based on a survey of the general population, the 1-year prevalence of vertigo is about 5%. For benign paroxysmal positional vertigo, the one-year prevalence is about 1.6%, and it is less than 1% for a vestibular migraine. The impact of vertigo should not be underestimated as nearly 80% of survey respondents reported an interruption in daily activities including employment and the need for additional medical attention.

Pathophysiology

Asymmetry in the vestibular system accounts for the symptom of vertigo. Asymmetry may result from damage or a dysfunction in the peripheral system such as the vestibular labyrinth or vestibular nerve or from a central disturbance in the brainstem or cerebellum. Though there may be a permanent vestibular disturbance the symptom of vertigo is never permanent as the central nervous system adapts over days to weeks.

History and Physical

The initial goal in diagnosis is determining whether or not the patient is truly experiencing vertigo as most patients will report dizziness as a chief complaint. A provider may ask "When you are dizzy, do you feel lightheaded or does it feel like the room is spinning around you?" True vertigo has been associated with an affirmative response to the latter portion of the question. Once vertigo has been identified, a thorough history helps the provider to differentiate between a central and peripheral etiology. Eliciting a time course of symptoms is one of the best ways to determine the underlying etiology. For instance, recurring vertigo lasting a few minutes or less is often associated with benign paroxysmal positional vertigo. A single episode lasting minutes to hours can be caused by a vestibular migraine or even a more serious underlying diagnosis such as a transient ischemic attack. More prolonged episodes can be seen in both peripheral and central causes such as vestibular neuritis or stroke.

Once a time course has been established, it is important to assess for associated symptoms as this can further help to differentiate a central from a peripheral etiology. Nausea and vomiting are typical with acute episodes of vertigo and are not specific for any particular etiology. Since it is important to rule out central causes that may be progressive or life-threatening such as a vertebrobasilar stroke or multiple sclerosis, providers must ask about any focal neurologic deficits such as diplopia, dysarthria, dysphagia, and numbness or weakness. An absence of any focal neurologic deficit does not completely rule out a serious central process, but its presence is very concerning and should be investigated further. Moving down the differential of central causes and associated symptoms, providers should inquire about symptoms of headache, photophobia, and visual auras as these often accompany vestibular migraines. There are numerous other symptoms associated with vertigo stemming from a peripheral lesion. Patients may experience deafness and tinnitus concerning for Meniere’s disease. They may report a recent viral infection which can cause acute labrynthitis and vestibular neuritis. Finally, it is important to review a patient's medication list and review social history for any substance or alcohol use. Medications that can affect vestibular function include anticonvulsants, salycilates, and antibiotics.

When combined with a complete history a focused physical exam can help further elicit a peripheral from a central cause of vertigo. Assessing for nystagmus is a key portion of the physical exam when a patient presents with vertiginous symptoms. A functional vestibular system allows us to maintain gaze during rotation through vestibular ocular reflexes. With a unilateral dysfunction in the vestibular system the eyes drift slowly away from a target and then correct with a fast movement in the reverse direction resulting in the appearance of a “beat” in the direction of the fast phase. In a peripheral vestibular lesion, the fast phase is away from the affected side and the frequency and amplitude of nystagmus will increase with gaze toward the side of the fast phase. For instance, a rightward gaze will increase a right-beating nystagmus. In peripheral lesions the predominant direction of nystagmus remains the same regardless of the direction of gaze while central lesions may present with nystagmus that reverses direction. Central lesions can present with nystagmus in any direction while peripheral lesions often present with horizontal nystagmus with a torsional component. It is important to note that nystagmus resulting from a peripheral lesion is never purely torsional or vertical. A physical examination technique to help further determine etiology is the head impulse or thrust techinique. In this exam, the patient is asked to keep their eyes fixed on a distant target with prescription eyeglasses if needed. The head is then turned quickly to the right or left by about 15 degrees. A normal response occurs when the eyes remain on the target. An abnormal response is when the eyes are dragged off of the target in the direction of the head turn followed by a saccade back to the target. This response implies a peripheral lesion resulting in a deficient vestibuloocular reflex on the side of the head turn. Finally, a provider may test for skew which involves the examiner covering one eye and observing for a vertical shift in the eye when uncovered. Central lesions sometimes produce a slight skew deviation. When the head impulse test is combined with an examination of nystagmus and a test for skew this is referred to as the HINTS (Head Impulse-Nystagmus-Test for Skew) test. A normal head impulse test on both sides with direction changing nystagmus or skew deviation is concerning for a central lesion. An abnormal head impulse test with unidirectional nystagmus and absent skew strongly suggests a peripheral lesion. The HINTS test may be more sensitive for the diagnosis of acute stroke than even MRI within the first 48 hours following symptom onset.

Other physical exam techniques may be used to diagnose and treat vertigo and include the Dix-Hallpike maneuver. It is the diagnostic test and treatment of choice when BPPV is suspected. Dix-Hallpike consists of 2 maneuvers. A patient sits on an exam table facing forward with eyes open, and the provider turns the patient's head 45 degrees to the right. The provider continues to support the patient's head while the patient lies back quickly to a supine position with the head hanging about 20 degreess off the end of the table. The patient remains in this position for 30 seconds before returning to the upright position where they are observed for another 30 seconds. This maneuver is repeated with the head turned to the left. The test is positive if at any point the maneuvers produce vertigo with or without nystagmus.

Gait and balance testing can further aid in localization. Patients with unilateral peripheral disorders often lean or fall toward the side of the lesion; whereas, patients with cerebellar lesions are often unable to walk without assistance and direction of falling with Romberg testing is variable.

The otoscopic exam should be completed to rule out an obvious infection such as acute otitis media, and bedside tests of hearing can be useful in differentiating other causes of vertigo. Weber and Rhinne tests are performed at the bedside to detect conductive and sensorineural hearing loss. However, audiometry is more sensitive than bedside testing in detecting hearing loss. A unilateral hearing loss points strongly to a peripheral etiology but if a cause can not be identified then further diagnostic imaging with MRI is warranted.

Evaluation

Laboratory testing is often not useful in identifying the etiology of vertigo. Diagnostic testing with brain imaging is indicated if a central lesion is suspected. Clinicians may find it difficult to distinguish between a central lesion such as infarction and a peripheral lesion such as vestibular neuritis in which the symptoms of vertigo can last for days. In this case, neuroimaging is recommended in patients with risk factors for stroke, associated focal neurologic deficits, a new headache and when the physical exam is not entirely consistent with a peripheral lesion. The modality of choice for is MRI and MRA as CT scans are less sensitive than MRI for the diagnosis and evaluation of central lesions.  However, if MRI is unavailable or contraindicated, a CT scan with thin cuts, particularly through the brain stem and cerebellum, may be used.

Treatment / Management

Treatment of vertigo is dependent upon the etiology, and often, treating the underlying etiology will improve the symptoms of vertigo.

Medications may be useful to suppress vestibular symptoms in acute episodes that may last a few hours to days. The most common medications used for symptomatic relief include antihistamines, benzodiazepines, and antiemetics. The most common antihistamine used is meclizine which is safe during pregnancy. Given sedating effects, caution is advised in using antihistamines, benzodiazepines, and antiemetics in elderly patients.

Additional non-pharmacologic treatments for patients with permanent unilateral or bilateral vestibular dysfunction include physical therapy with vestibular rehabilitation. Vestibular rehabilitation exercises train the brain through alternative visual and proprioceptive clues to maintain balance.  Several randomized control trials have shown benefits in vestibular rehabilitation including a decrease in vertiginous symptoms, a decrease in movement provoked dizziness, and improvement in activities of daily living.

In some patients, particularly those diagnosed with vestibular neuritis, a combination of pharmacologic and nonpharmacologic therapy is recommended. In vestibular neuritis, steroids are recommended in the acute setting in addition to vestibular rehabilitation. In patient's with Meniere’s disease, lifestyle adjustments in addition to medication and vestibular rehabilitation have shown to be effective.

Patient's with Meniere’s disease may be particularly sensitive to a high salt diet, caffeine, and alcohol. Avoiding known triggers can help to alleviate symptoms. Diuretics may also be prescribed when diet modification alone is not sufficient in controlling symptoms. Acute episodes can be symptomatically treated with vestibular suppressants like meclizine.

Patients with benign paroxysmal positional vertigo benefit from non-pharmacologic agents. The primary treatment for BPPV is focused on head rotation maneuvers that displace calcium deposits back to the vestibule through Canalith repositioning or the Epley maneuver. The benefit of the Epley maneuver is that the patient at home can perform it. To perform a modified Epley maneuver, instruct the patient to position themselves upright on a bed with their head turned 45 degrees to the left and a pillow behind them. The pillow should be positioned so that when supine the pillow is directly under their shoulders. Once the patient is in position, they should like back quickly onto the pillow so the head is reclined onto the bed. They should hold this position for 30 seconds. Without raising their head, they should then turn their head 90 degrees to the opposite side (right) and hold this position for another 30 seconds. After 30 seconds, they should turn their body and head another 90 degrees to the right and wait for another 30 seconds. Finally, they should sit up on the right side of the bed. This maneuver can be repeated starting on the opposite side and should be performed at least three times a day until the patient has no further episodes of positional vertigo for 24 hours. Unfortunately, BPPV is intractable in a select number of patients, and surgical treatment can be an option, particularly if symptoms are disabling. Surgical options include occlusion of the posterior canal with bony plugs or transection of the posterior ampullary nerve. Either surgical procedure has risks of hearing loss.

Differential Diagnosis

The differential diagnosis of the symptom of vertigo is extensive as it can arise from a central or peripheral lesion in the vestibular system. Therefore, it is important to differentiate vertigo from symptoms of disequilibrium and pre-syncope such as imbalance and lightheadedness. An extensive list of metabolic, vascular, inflammatory, iatrogenic, and endocrine causes can lead to these symptoms.


References

[2] Initial evaluation of vertigo., Labuguen RH,, American family physician, 2006 Jan 15     [PubMed PMID: 16445269]