Vestibular dysfunction is a disturbance of the body's balance system. The disorder differentiated into peripheral and central causes. The symptoms of peripheral and central vestibular dysfunction can overlap, and a comprehensive physical examination can often help differentiate the two. Vestibular disorders usually present acutely. The patient's symptom complex typically consists of vertigo, nausea, vomiting, intolerance to head motion, nystagmus, unsteady gait, and postural instability. The most common form of acute peripheral vestibular dysfunction is vestibular neuronitis. The most common cause of severe central vestibular dysfunction is an ischemic stroke of the posterior fossa, which contains the brainstem and cerebellum. An acute ischemic stroke accounts for up to 25% of patients who present as central vestibular function. Since acute stroke is treated differently, it is essential to recognize this disorder. The second common cause of central vestibular dysfunction is a demyelinating disease. Studies have shown there is a small prevalence of vestibular dysfunction in patients with syncope. Syncope is a presentation of vertebral basilar artery disease with a prevalence of five percent of strokes. Symptoms of vestibular dysfunction include a variety of symptoms: vertigo, nausea and vomiting, intolerance to head motion, spontaneous nystagmus, unsteady gait, and postural instability caused by injury to peripheral or central vestibular structures. The prevalence of each of these symptoms varies, and there is no single symptom that helps identify vestibular dysfunction. The predominance of the symptoms listed above as a cluster leads to the suspicion of vestibular dysfunction. The history and physical exam is the way to differentiate peripheral from central vestibular dysfunction.
It is necessary to identify which type of vestibular dysfunction a patient has, as this determines the therapeutic approach. The mainstay treatment for peripheral disorders is symptomatic therapy with anticholinergic medications or type 1 antihistamines. The treatment for central vestibular dysfunction caused by an ischemic stroke can include intravenous thrombolytic therapy and interventional clot retrieval in the hyperacute phase and stroke secondary prevention after that. The early identification of demyelinating disorders such as multiple sclerosis is essential so that treatment can be initiated to prevent the rapid decline and development of disabilities. This article will review the epidemiology, history and physical examination, evaluation, differential diagnosis, treatment, complications, and critical points in improving the identification of vestibular dysfunction, and differentiating peripheral from central vestibular disorders.
The etiology of vestibular dysfunction can be divided into peripheral and central causes.
The constellation of symptoms, which include vertigo, nausea, vomiting, head motion intolerance, unsteady gait, and postural instability, signify an acute vestibular syndrome. The symptoms persist for at least 24 hours, except in paroxysmal positional vertigo.
Paroxysmal positional vertigo is a mechanical disorder of the inner ear causing short intervals of transient vertigo, often with autonomic symptoms. Benign positional peripheral vertigo accounts for up to 8% of individuals with moderate to severe dizziness/vertigo. Women and patients over age fifty are among the most affected. The average duration of symptoms is two weeks. It is caused by the inactivation of the semicircular canal, usually the posterior semicircular canal, and typically only affects one side. This is generally due to the presence of free-floating particles that form a clump in the posterior semicircular canal when the head changes position. The endolymph motion is moved in a plunger fashion, causing displacement of the cupola. This produces the symptoms of dizziness described as spinning. These symptoms are most obvious with changes in position and are usually worse in the morning. Positional paroxysmal vertigo is known as a particle disease.
Vestibular neuronitis is another peripheral vestibular disorder. It is believed to be caused by an acute viral or post-viral inflammatory disorder. The viral-induced inflammation affects the vestibular branch of the eighth cranial nerve.
The third peripheral vestibular disorder is Ménière disease. This is associated with endolymphatic hydrops with distortion and distention of the endolymph portions of the labyrinthine system. Most patients have no underlying otologic disease. The causes of the excess fluid in the labyrinthine system have been difficult to determine, but there are six proposed etiologies. One of the etiologies is the blockage of the endolymphatic sac or duct. The entrance of the endolymphatic sac becomes blocked by saccular otoconia (calcium crystals) that detach from the membranes and block the flow of endolymph. This is the same mechanism proposed for paroxysmal positional vertigo. The second theory is a hypoplasia of the vestibular aqueduct. The third is an immunologic mechanism that has not been clearly defined. Fourth is a genetic predisposition through an autosomal dominant inheritance pattern. This cause is present in 8% to 15% of patients with Ménière disease in two studies. A family history of an earlier age onset is helpful. The studies showed more severe manifestations in successive generations. However, a specific gene marker has not been identified. A fifth etiology proposed is a viral cause. The viruses suspected are herpes simplex, varicella-zoster, and cytomegalovirus. Studies in which endolymph fluid samples were taken at surgery were not able to detect viruses. Finally, the sixth etiology proposed occurs in patients with migraines and who have Ménière disease. As migraines have a vascular origin, it has been postulated that for two disorders, Ménière disease is suspect. Another theory studied and elaborated upon approximately 50 years ago proposes that the rupture of the dilated or distended endolymphatic sac allows potassium-saturated endolymph into the perilymphatic space. The result is that the biochemical gradient depolarizes the cochlear and vestibular hair cells, leading to loss of function. Once the gradient is restored to normal, by equalizing the gradient, the membrane rupture seals and the ion pumps normalize the hair cells' function. This process repeats and results in the degeneration of the hair cells, which has been shown on cytologic evaluation. Trauma to the ear can also cause vestibular damage.
The central vestibular causes are a vertebrobasilar transient ischemic attack (TIA) affecting the cranial nerve VIII, acute ischemic stroke involving the vestibular nerve tracts, cerebellum, or brainstem, hemorrhagic stroke affecting the brainstem and cerebellum, demyelinating diseases that affect the vestibular tracts, cerebellum, and brainstem such as multiple sclerosis, etc. Another etiology is a brain injury affecting the cerebellum and brain stem. The symptoms of stroke affecting this area, brain stem, and cerebellum have similar symptoms of vertigo, nystagmus, nausea and vomiting, and gait. As stated earlier, stroke is present in 25% of those with dizziness. Medications such as aminoglycosides can affect the vestibular nerve tracts. The history and physical exam are important in identifying the causes of vestibular dysfunction.
Vestibular dysfunction often presents as dizziness. Dizziness is a common complaint of patients 40 years and older, leading to 10 million visits to ambulatory care settings, and 25% of emergency department visits. Vestibular dysfunction has an association with stroke and demyelinating diseases. Twenty-five percent of patients with vestibular disorders have had a stroke. Patients with vestibular dysfunction are at higher risk for falls due to vertigo and gait imbalance. Falls are a cause of injury in patients 70 years and older. The 1-year prevalence of vestibular dysfunction is 4.9%, while lifetime prevalence is 7.4%. Risk factors that increase the risk of Vestibular dysfunction include female gender, lower educational level, age above 40, cardiovascular disease, and depression.
The history and physical exam can help identify the clinical presentation of the various causes of the symptoms of vestibular dysfunction. It can also determine the need for diagnostic testing. The history should focus on the timing onset and the presence of symptoms for at least 24 hours. The history should define and clarify the vague symptoms of dizziness to syncope. Open-ended questions and giving the patient the ability to describe and confirm their symptoms helps. Each symptom should be defined as it relates to vestibular and cerebellum disturbances. Dizziness needs to be defined, whether it relates to balance. The classical spinning sensation does not have to be described; it can be a swaying or a tilting sensation. The patient may describe it in vague terms of imbalance or disorientation. Swaying is not to be confused with woozy or faint feeling. The patient usually has nystagmus with these symptoms on a physical exam. The severity of nystagmus and the pattern can help differentiate peripheral from a central vestibular disorder. Tilt illusion in patients has a feeling of leaning or sometimes upside down. Tilt illusion is related to the otolithic organs' function. The otolithic organs' dysfunction may cause lateral propulsion (the tendency to fall to the side of the lesion). The patient can describe oscillopsia, the visual illusion of a to and from motion and blurred vision when the head is in motion. Otolithic dysfunction can signify an impairment of the vestibular-ocular reflex. Patients can have drop attacks, which are the feeling of being pushed or pulled to the ground. There is no presyncope or feeling of going to faint with drop attacks. They can be a sign of loss of tone mediated vestibulospinal reflexes. They may also be associated with Ménière disease and aminoglycoside toxicity. Patients with postural and gait instability, and examination findings of vertigo, signify vestibular nuclei dysfunction and will affect antigravity muscles that maintain posture.
The history of the evolution of symptoms over time is important. Vertigo is usually not continuous or long-lasting with vestibular etiology. The central nervous system adapts, and vertigo subsides over days or weeks. If the clinician obtains a history of constant vertigo or dizziness lasting months, it is not vestibular. The clinician has to make sure the patient is not referring to the constant ringing in the ears, as this is consistent with vestibular dysfunction for etiologies, such as Ménière disease. The length of the episodes is the best way to identify the causes of vestibular dysfunction. Recurrent episodes lasting under one minute are usually paroxysmal positional vertigo. A single episode of vertigo lasting several minutes to hours may be due to a migraine or transient ischemic attack that is related to the vascular areas of the labyrinth or brainstem. Recurrent episodes that last hours, but seem briefer, are associated with Ménière disease. They can also be associated with mechanisms of the peripheral vestibular areas described as physiologic explanations for Ménière disease, sometimes referred to as vestibulopathy. The lasting vertigo days with several episodes can occur with vestibular neuronitis, multiple sclerosis, infection of the brainstem, or cerebellum.
History of aggravating and provoking factors must be obtained. Vertigo that worsens with head motion implies vestibular causes. Aggravating symptoms of coughing, sneezing, exertion, or loud noises raise the suspicion of perilymphatic fistula. Perilymphatic fistula is an abnormal connection between the middle ear and the perilymphatic space of the inner ear resulting from superior canal dehiscence. The condition allows the pressure from the cerebrospinal fluid space to the inner ear. Patients at high risk of perilymphatic fistula include those with a history of a traumatic event from diving or flying, vestibular surgery, symptoms worsening with straining in bowel movements, or weight lifting. A history of hyperextension injury of the neck points to vertebral artery dissection, which presents with persistent neck pain. A recent viral illness or symptoms can help identify vestibular neuronitis as etiology.
Associated symptoms with vertigo are also helpful in identifying etiology. Patients presenting with vertigo, diplopia, dysarthria, weakness, or numbness should be evaluated for central nervous system etiologies like acute ischemic stroke and demyelinating disorders like multiple sclerosis. The neurologic symptoms may precede or follow vertigo. Ménière disease often has deafness and tinnitus. There can be a sensorineural hearing loss from trauma, which causes a perilymphatic fistula. Headache, photophobia, and phonophobia suggest migraines with vertigo.
Past medical history should be obtained and can help identify the etiology. Vascular risk factors such as hypertension, diabetes mellitus, smoking increase the likelihood of stroke. Studies have found that vertigo with two or more risk factors has an 8% risk of stroke in 2 years. Those patients with three or more risk factors and vertigo have a 14% 2-year risk of a stroke. Prior history of migraine, patterned with vertigo, tend to be a vestibular migraine. Head trauma can be a precursor to paroxysmal position vertigo or perilymphatic fistula. Usage of medication such as aminoglycosides, chemotherapeutic medications (cisplatin) can cause vestibular toxicity and cause vestibular symptoms of peripheral etiology. Long term use of seizure medications like phenytoin and Tegretol can affect the cerebellum centrally.
Physical examination can help define the nystagmus. Additionally, specific physical exam testing such as Dix-Hallpike maneuver, head impulse test, skew deviation, hints exam, ocular tilt reaction, and similar tests should be performed. These tests help to differentiate peripheral from central etiologies. Weber and Rinne tests can be used to distinguish conductive and sensorineural hearing loss. The mixed horizontal-torsional nystagmus results if a peripheral lesion affects all three semicircular canals on one side. Visual fixation tends to suppress nystagmus that is due to a peripheral lesion, but not a central lesion. There are many types of nystagmus. Spontaneous nystagmus is a slow drift of the eyes away from the target in one direction and is followed by a fast corrective movement in the reverse direction. The asymmetry of the vestibular activity continues until the peripheral vestibular activity has returned to normal, and central nervous system activity has adapted to the vestibular lesion. Nystagmus can be physiologic or pathological. Physiologic is a form of involuntary eye movement, as stated earlier, and is part of the vestibular ocular reflex (VOR). The movements of the eyes are smooth, alternating in one direction and saccadic movement in the other direction, which is generally horizontal. Pathological nystagmus is produced by an abnormality of the central or peripheral ocular vestibular reflex response. It can also be the result of a response in the central or peripheral ocular vestibular symptom form a stimulus outside of the motion of the head, such as caloric water stimulation.
The following tests are important, and clinicians must know how to perform and interpret them.
Rinne and Weber tests: The Rine and Weber tests are used to evaluate conductive and sensorineural hearing using a tuning fork, vibrating at 512 HZ, and are done at the bedside. The Weber test is normal when the vibration sound is heard equally in both ears. In sensorineural hearing deficits, the sound lateralizes to the normal ear. With conductive hearing deficits, the vibration sound lateralizes to the affected ear.
The Rinne tests look for conductive hearing loss. It differentiates between air conduction and bone conduction loss. Normally, air conduction is better than bone conduction, and the patient hears the sound louder next to the ear than when placed on the mastoid bone. In sensorineural deficits, both air and bone conduction loss is demonstrated. However, air conduction remains better than bone conduction. With the conductive hearing deficit, the sound heard is better heard on the mastoid compared to the ear. Identifying unilateral sensorineural hearing loss localizes the lesion to a peripheral etiology. Audiometry would be the next step to confirm this. Evaluation of the internal auditory canal and posterior fossa is part of the evaluation.
Dix-Hallpike-maneuver: Dix-Hallpike maneuver is the use of a positional change to reproduce vertigo and produce nystagmus in patients with positional dizziness. The test is best for patients who are not dizzy or vertiginous at rest. This test identifies benign paroxysmal positional vertigo. It tests for posterior canal dysfunction in the lower ear. The nystagmus and vertigo disappear after a latency period and when the patient is in the supine position. After the patient sits up, the nystagmus will be in the opposite direction. The clinician repeats the maneuver to the same side, and each time the intensity and duration of nystagmus diminish. The repetition confirms the fatigable nature of the phenomenon. The delayed onset of nystagmus for 30 seconds, transient and diminishing response on repeat, and the type of nystagmus described above are significant for benign positional paroxysmal vertigo. The sensitivity for identifying this condition is in the range of 88 percent.
Head impulse test (HIT): HIT is for differentiating vestibular dysfunction for non-vestibular dizziness. The clinician performs the HIT by the patient keeping his or her eyes focused forward on an object/target. At the same time, the clinician turns the head, followed by a repetitive motion to the original position. The normal response the eyes remain focused on the object. The abnormal response is the eyes are dragged off the target in the direction in which the head is rotated. The abnormal response signals a deficient vestibular-ocular reflex on this side of the head is turned and implies peripheral lesion. The test is 82 to 100 percent specific and 34 to 39 percent. Sensitivity is increased by flexing the head 30 degrees during the maneuver ( 71% to 84%). The test has been helpful in patients presenting with prolonged vertigo and differentiating between peripheral and central lesions. It is abnormal with vestibular neuritis and normal with cerebellar infarction. Exceptions exist with infarctions of the eighth cranial nerve or inner ear.
Skew deviation: Skew deviation is another test identifying central lesions in the brainstem. The vertical alignment of the eyes is off relative to the ocular motor nuclei. A red lens is placed over one eye, shining a white point of light at the patient and asking the patient to note the relative position of the red spot to the white point of light. The clinician moves the white point of light to see how the separation changes with the lateral and vertical gaze. With Skew deviation, gaze direction has little effect upon the distance between images, which is termed commitment. If the gaze is incompetent, then cranial nerve IV palsies need to be considered.
HINTS examination: The Hints examination is an exam combining the Head Impulse test (HIT) with the Skew test. The presence of normal HIT and skew deviation suggests central rather than peripheral vertigo.
Ocular tilt reaction: The patient has a triad of skew deviation, a torsional tilt of the eyes with the upper poles tilted toward the lower, and head tilt toward the eye is lower. Ocular tilt can occur with acute peripheral lesions or central lesions involving the cerebellum or brainstem vestibular pathway. Besides the ocular tilt test and skew, the tilt of subjective visual vertical, which is a sensitive sign of static vestibular imbalance, is used to help in the differentiation discussed above.
Head-shaking visual acuity is a test where the patient reads the eye chart while the head has been shaken and then reads the eye chart while not shaking the head. If the shaking acuity is more than four lines worse than the head shake, acuity indicates poor vestibular ocular reflex.
Head shaking nystagmus is used to test for unilateral vestibular lesions. One instructs the patient to shake head side to side with eyes closed for 15-40 seconds, causing stimulation of the horizontal semicircular canals of both sides. When the patient stops shaking the patient opens his or her eyes and looks straight ahead. If both sides were equally stimulated, the response is balanced, leaving the eyes to be still. If there is unilateral labyrinthine damage, there will be nystagmus that beats away from the damaged side. The test can be normal in patients with bilateral damage. The sensitivity is 46 percent and specificity 75 percent. If there is a central lesion in the medullary region, the nystagmus is toward the same side of the lesion. The Head-shaking nystagmus test has been found in one study to be present in 85% to 100% of patients with vestibular neuritis.
The evaluation of patients with vestibular dysfunction is usually determined by the examination testing includes brain imaging by magnetic resonance imaging (MRI), computed tomography (CT), electronystagmography (ENG), videonystagmography (VNG), Vestibular-evoked myogenic potentials (VEMP), and brainstem auditory evoked potentials (BAEP). These tests are not always needed due to the low yield and the expense associated with the test.
Magnetic resonance imaging of the brain is indicated when history and physical exam tests like HIT, Skew deviation, HINTS, Dix-Hall Pyke maneuver, and vestibular exams identify a central cause. Patients with risk factors for stroke, neurologic signs, and symptoms should have neuroimaging to evaluate for acute ischemic stroke. Young patients who have acute sustained vertigo, with no risk factors for stroke, no neurologic signs or symptoms, suppression with visual fixation, falling opposite direction to nystagmus, and horizontal with torsional nystagmus do not need immediate imaging unless symptoms persist for 48hours. MRI brain can detect acute ischemic stroke with a very high sensitivity and specificity. CT head has low sensitivity for strokes infarct and other lesions in the brainstem. CT head has a high sensitivity for intracranial hemorrhage and is more readily available in most places and can be done emergently and is often the initial screening test when evaluating for stroke.
Treatment of vestibular dysfunction depends on the etiology. Symptomatic management is the mainstay for most patients. These include antiemetics (metoclopramide, ondansetron, prochlorperazine, promethazine), vestibular suppressant medications (diphenhydramine, dimenhydrinate, meclizine), benzodiazepines (alprazolam, clonazepam, diazepam, and lorazepam), etc.,
Benign positional vertigo using the Epley maneuver, which involves placing the patient head indifferent position to rotate endo-crystals in to correct position and release the blockage. Other maneuvers such as Semont, half-somersault, foster maneuver, and Brandt-Daroff exercise are also sometimes used. The clinician use such maneuvers to reposition the endolymph and crystals to restore the flow and correct the peripheral structural lesion.
Goals of treatment for Ménière disease are the reduced frequency and severity of vertigo attacks, reduce or eliminate hearing loss and tinnitus associated with attacks, alleviate chronic symptoms, and minimize disability. Treatment options include lifestyle changes and avoiding triggers. A low sodium diet of 2 to 3 gm per day, limiting caffeinated beverages, alcohol, nicotine, stress, monosodium glutamate, and allergens can help.
Classification of the vestibular dysfunction as peripheral or central is important in determining the diagnosis. Central nervous systems should be considered when patients present with vertigo and dizziness, where the examination shows a pattern of nystagmus that is persistent down beating, pure torsional, or refractory to repositioning. Disorders of cerebellar, brainstem or medulla infarction, cerebellar tumor, Chiari malformation, multiple sclerosis, migraine vertigo, and degenerative ataxia disorders are considerations.
Peripheral vestibular dysfunction is identified by nystagmus that is responsive to repositioning maneuvers. The conditions to consider are benign paroxysmal position vertigo, vestibular neuritis, endolymphatic disorders, and Ménière disease.
The prognosis of vestibular lesions depends upon the etiology. Benign paroxysmal position vertigo has a fair prognosis but often recurs. Ménière disease is characterized by recurrent attacks and progressive disease at times, which results in both hearing loss and balance issues that lead to disability. Treatment of symptom control and rehabilitation with lifestyle changes delay disability overall. Central lesions prognosis is fair as the patient often responds to rehabilitation overtime, but disability from the balance or other effects of stroke can be debilitating.
Specialist consultation from neurology and/or otolaryngology and additional tests like ENG, VNG, VEMP, audiometry, and BAEP are reserved for outpatient settings. They combine these tests with HIT and caloric testing to discriminate peripheral and central etiologies. VEMP can be useful for the detection of superior semicircular dehiscence syndrome. BAEP can be used to detect acoustic neuromas.
Vestibular dysfunction can contribute to symptoms of varying severity and frequency. Patient education must be an important part of the clinical management of patients with vestibular dysfunction. The initial focus must be on accurate diagnosis based on a detailed history, comprehensive physical examination, and supporting diagnostic testing. Once the diagnosis is established, counseling must be given about the diagnosis and prognosis. Creating an individualized care plan can empower the patient. Appropriate use of symptomatic medications and counseling of side effects and monitoring for drug interactions must be performed.
Benign paroxysmal positional vertigo has a time course of recurrent brief seconds. Patients often present with predictable head movements or positions that precipitate symptoms. The nystagmus is characteristic of peripheral as identified by the Dix-Hallpike maneuver. There was no associated neurologic symptoms or auditory sensory symptoms. Epley's maneuver and other similar maneuvers treat the condition. There is a treatment for recurrence with antiemetics and vestibular suppressants.
Vestibular neuritis presents with a single acute episode onset and last days; there may be a viral syndrome accompanying or preceding vertigo, The nystagmus is peripheral characteristics, and HITS/head-shaking nystagmus tests are abnormal. The patient has associated neurologic symptoms of falls toward the side of the lesion, but no brain stem symptoms and usually have no auditory symptoms.
Ménière disease presents with recurrent episodes that last minutes to several hours. The attacks are spontaneous in onset. The nystagmus is peripheral. There are no associated neurologic symptoms. Patients have associated auditory sensory symptoms of ear fullness and or pain, vertigo, unilateral hearing loss, and tinnitus. Audiometry shows a unilateral low-frequency sensorineural hearing loss. The clinician uses Weber and Rhine's tests to determine audiometry indication.
A vestibular migraine may present in patients with a history of migraine. There is a history of recurrent episodes that last several minutes to hours. The nystagmus can have characteristics of central or peripheral. A migraine headache may have other symptoms or prodrome accompanying vertigo that could be neurologic. Usually has had prior normal testing and history of relief with migraine medications.
Vertebrobasilar TIA presents as a single or recurrent episode lasting several minutes or hours. It occurs in older patients with vascular risk factors and or cervical trauma. The nystagmus is central if present. The symptoms are lateral medullary. MRI and MRA may demonstrate vascular lesions.
Patients with brainstem infarction present with sudden onset and persistent symptoms over days to weeks. These are older patients with vascular risk factors. The nystagmus is central. The presentations are associated with neurologic symptoms of the medullary (ataxia). The patients do not have auditory sensory symptoms unless the anterior inferior cerebellar artery is involved. The patients will demonstrate a lesion on MRI.
Patients presenting with cerebellar infarction or hemorrhage have a sudden onset and persistent symptoms over days to weeks. These patients have vascular risk factors such as hypertension. The nystagmus has central characteristics. The patient has associated neurologic gait impairment and headache. The patient presents with abnormal limb coordination described as overshoot or undershoot of the intended position with hand, arm, or leg. MRI will identify the lesion, and CT will also as symptoms have present for days or hemorrhagic illness is present.
An interprofessional team that provides a holistic and integrated approach to postoperative care can help achieve the best possible outcomes. Early recognition of patients presenting with vertigo and dizziness when having central symptoms is important. The clinician needs to be familiar with the bedside examination that differentiates peripheral from central etiologies. Clinicians should not rely on history alone. In addition, they should define the type of dizziness and recognize that nonspecific dizziness and lightheadedness are associated with stroke, similar to peripheral vertigo. A central nervous system cause should be considered whenever the pattern of nystagmus is persistent down beating, pure-torsional, or when it is refractory to repositioning maneuvers. When symptoms are persistent over 48 hours, or other neurologic signs are present, an MRI of the brain should be strongly considered. Collaboration, shared decision making, and communication are key elements for a good outcome. The interprofessional care provided to the patient must use an integrated care pathway combined with an evidence-based approach to planning and evaluation of all joint activities.
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