The term vestibular disorder (VD) means the condition is related to vestibular structure (peripheral and central) or its mechanism. On the other hand, vestibular symptoms or dysfunctions are broader terminologies and include symptoms not related or partially related to vestibular apparatus or mechanism.
Key points
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Vestibular disorder is a dysfunction in the balance system of the body either due to malfunctioning of the inner ear or due to central nervous system dysfunction or both.
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Vestibular neuritis is defined by an acute onset of vertigo for 24 hours or more without hearing loss.
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Typical symptoms of vestibular dysfunctions include vertigo, vestibulo-visual symptoms, postural symptoms, and tinnitus.
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Common types of acute peripheral vestibular dysfunction include benign paroxysmal positional vertigo, vestibular neuritis, Ménière’s disease, and vestibular migraine.
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Demyelinating disease such as multiple sclerosis and ototoxic medications can also cause vestibular symptoms.
Introduction to vestibular disorders
The term vestibular disorder (VD) means the condition is related to vestibular structure (peripheral and central) or its mechanism. On the other hand, vestibular symptoms or dysfunctions are broader terminologies and include symptoms not related or partially related to vestibular apparatus or mechanism. Vestibular system consists of (a) peripheral vestibular structures located in the inner ear (balance system), which include the utricle, the saccule, and 3 semicircular canals (lateral, superior, and posterior) and (b) brainstem and cerebellum (processing centers). Together with visual and somatosensory systems, structures of the inner ear fire signals to the central nervous system (CNS) to maintain balance, and orient head and body in space. If a lesion is in the inner ear, it is classified as peripheral vestibular disorder, and if a lesion is in the CNS, it is known as central vestibular disorder.
This review article focuses mainly on the diagnosis and management of the common peripheral VD such as benign paroxysmal positional vertigo (BPPV), Ménière’s disease, vestibular migraine, and vestibular neuritis.
Both central and peripheral VD can be acute (up to 2 weeks), subacute (up to 3 months), and chronic (more than 3 months). Detailed history and physical examinations aid in identifying the type of VD, which is critical in managing different types of VDs. Estimated 33 million adults and 3.5 million children and adolescents in the United States are affected by VD.
Etiology of vestibular disorders is multifactorial. Depending on the etiology of vestibular disorder, symptoms may vary. Symptoms of central and peripheral vestibular disorders usually present acutely and include vertigo, tinnitus, nausea, vomiting, unsteady gait, fall, and nystagmus. , Symptoms of acute vestibular disorders may last from a week to few months and may become chronic. For example, unilateral vestibular nerve pathology may cause nystagmus, dizziness, gait disturbance, and sensation of dizziness with head movement. Nystagmus and dizziness in unilateral vestibular nerve impairment may last 1 to 2 weeks, but unsteady gait may last weeks to months. More than 1 vestibular disorder may occur simultaneously in some patients. Vestibular migraine may co-exist with BPPV, and Ménière’s disease may co-exist with vestibular migraine. In general, patient education and appropriate symptomatic treatments may be enough in managing vestibular disorders of peripheral origin, whereas treatments for the central vestibular disorders are disease-specific. Management of peripheral VDs includes pharmacotherapy, vestibular rehabilitation, psychotherapy, and rarely surgery. Kamo and colleagues have reported that early vestibular rehabilitation improved several measured outcomes in patients with acute vestibular disorders. Often pharmacotherapy is started without a definite diagnosis for the symptomatic treatment of vestibular disorders. Because of the broad differential diagnoses of VDs, a multidisciplinary approach may be needed when managing patients with VDs. Vestibular disorders if not managed properly can increase risk of fall, loss of workdays, and may adversely affect quality of life of the patients.
Vertigo, dizziness, and tinnitus
Vertigo, dizziness, and tinnitus are frequent causes of primary care, emergency room visits, and referral to a consultation. The International Classification of Vestibular Disorders of the Bárány Society defines vertigo as a sensation of self-motion when no self-motion is occurring or the sensation of distorted self-motion during an otherwise normal head movement. It defines dizziness as a sensation of altered spatial orientation without the feeling of false motion. According to this classification, vertigo is considered a separate entity but not a type of dizziness. Vertigo and dizziness are common symptoms of vestibular disorders. Both can be spontaneous without obvious triggers or triggered with an identifiable cause. Common triggers of vertigo are position of the head, head movement, sound, visual (seeing objects in motion), straining (Valsalva maneuver), and orthostatic. Peripheral vertigo is most common in BPPV followed by Ménière disease and vestibular neuritis. Tinnitus is a perceived sound in the absence of an internal or external source. Tinnitus is usually benign in nature. While there is no universal cause of tinnitus, risk factors include sensory neural hearing loss, loud noise exposure, trauma, infection, and medications. Evaluation begins with a history and physical, followed by audiology evaluation. There is no cure for tinnitus, however, there are treatment strategies that can be utilized to alleviate symptoms and improve quality of life. These treatment options encompass directed attention and habituation through various methods including, but not limited to, tinnitus retraining therapy, cognitive behavior therapy, tinnitus activities treatment, and progressive tinnitus management.
Benign paroxysmal positional vertigo
As the name suggests, BPPV is characterized by a brief, spinning sensations elicited by a change in the position of the head and lasts few seconds. According to the American Academy of Otolaryngology-Head and Neck Surgery Foundation Clinical Practice Guideline, diagnostic criteria for posterior canal BPPV are repeated episodes of vertigo with changes in head position and vertigo associated with nystagmus that is provoked by the Dix-Hallpike test. It is important to keep in mind that there is a latency period of about 60 seconds between the completion of the Dix-Hallpike test and the onset of vertigo and nystagmus. Besides being the most common cause of vertigo, BPPV is also the most common vestibular disorder in adults. About 42% of patients with vertigo are diagnosed with BPPV. It is more common in females than in males (2:1) and with a peak onset between 50 and 70 years of age. Vertigo in patients with BPPV is brief, lasting between 30 and 60 seconds, and triggered by a change in the position of the head relative to gravity, such as tilting one’s head back, rolling over in bed, or going down to or getting up from the bed. In addition to vertigo, BPPV may lead to nausea, vomiting, decreased work performance, depression, and fall which could be partly due to a reported association of BPPV with osteopenia or osteoporosis. BPPV is not associated with hearing loss. Often, BPPV is underdiagnosed or even misdiagnosed.
Underlying pathophysiology of BPPV is a free-floating otoconia (canalithiasis) entering one of the semi-circular canals, mainly posterior semicircular canal (up to 90% of all cases), followed by horizontal and then anterior semi-circular canal. Detached otoconia from the utricular otolith, now reside in one of the semi-circular canals, and move to a new position with the movement of the head, creating a false sensation of rotation. ,
BPPV usually is unilateral, but bilateral and multiple canals BPPV have been reported but it is rare. Most cases of BPPV are idiopathic. Head injury, vestibular neuritis, and Ménière’s disease have been reported to lead to BPPV. Prognosis of BPPV is usually very good with many cases going into spontaneous remission within 12 weeks, especially if the horizontal semi-circular canal is involved. Although, BPPV may last a few weeks, but each episode of BPPV lasts only for a few seconds.
Differential diagnosis of BPPV includes stroke, vestibular neuritis, vestibular migraine, Ménière’s disease, and labyrinthitis. A thorough history, physical examination, medication review, and additional appropriate testing may help identify the underlying cause of acute episodic vertigo. According to BPPV guideline evidence-based statements, “Clinician should diagnose posterior semicircular canal BPPV when vertigo associated with nystagmus is provoked by the Dix-Hallpike maneuver, performed by bringing the patient from an upright to supine position with the head turned 45° to one side and neck extended 20°” (Strong recommendation). The Dix-Hallpike maneuver is considered the gold standard test to diagnose posterior canal BPPV and should be performed bilaterally to determine which side is involved and to find out whether it is unilateral or bilateral. Patients with certain co-morbid conditions such as cervical stenosis, severe rheumatoid arthritis, morbid obesity, and others are at increased risk of complications from the Dix-Hallpike maneuver. Dix-Hallpike maneuvers should not be performed if a patient has neurologic signs or symptoms, and a patient is dizzy when still. Patients with a high index of suspicion for BPPV in whom Dix-Hallpike test is negative, should be tested for horizontal or lateral semi-circular canal BPPV using supine roll test. The technique to perform supine roll test can be viewed at https://www.youtube.com/watch?v=U3SGJfjwJaw .
Treatment of posterior canal benign paroxysmal positional vertigo
Although spontaneous resolution of BPPV is possible within few weeks from the time of onset, recovery can be expedited using particle repositioning maneuver (PRM). Epley (canalith repositing procedure) and Semont (liberatory) maneuvers are the 2 most used PRM in clinical practice and can be performed in the office. Both techniques are therapeutic may eliminate vertigo due to BPPV. Number of times a patient may have to undergo PRM varies from 1 to many with no reported optimal numbers. Techniques to perform Dix-Hallpike maneuver and Semont maneuver are shown in Figs 1 and 2 , respectively. The Semont maneuver can be substituted with Epley’s maneuver. Before performing any of these maneuvers, patients should be made aware of possible worsening of vertigo, nausea, and vomiting. Anti-emetic medications may be prescribed in some patients before the procedure based on shared decision-making.
Steps to perform Epley’s maneuver can be viewed at https://www.youtube.com/watch?v=LxD-lgqix-s .
Vestibular rehabilitation (VR) which is performed by a trained physical therapist can be used as initial therapy for BPPV. Patients with persistent BPPV should be re-evaluated for alternative diagnosis as central nervous system disorder may co-exist with BPPV. Surgical treatment for BPPV is rare and needed for cases refractory to PRM or VR. It is not recommended to routinely prescribe vestibular suppressant therapy like antihistamines or benzodiazepine.
Vestibular neuritis or vestibular neuronitis
Vestibular neuritis (VN) is characterized by an acute onset of spinning vertigo lasting at least for 24 hours without hearing loss and central neurologic signs. Most patients with VN are between 40 and 70 years of age. Rotational vertigo in VN peaks on the first day and patients usually prefer lying down on the side with the healthy ear over the pillow, which may improve over the period of few days.
Etiology of VN is unknown. Viral infections (coronavirus disease 2019 [COVID-19] and human simplex virus type 1) and adenoviral vector-based COVID-19 vaccines, , autoimmune disorder affecting vestibular nerve, and vestibular artery ischemia are proposed etiologies of VN. Secondary BPPV could be a result of VN, although the exact relationship between the 2 is unknown.
Diagnosis of vestibular neuronitis
Sustained rotational vertigo in VN may be preceded by spells of episodic vertigo few days prior. Vertigo is often accompanied by spontaneous peripheral horizontal vestibular nystagmus, nausea with or without vomiting, and ataxia. Ataxia in VN is manifested as body tilting to the diseased side and may result in fall. Tinnitus, ear pain, diplopia, recent trauma, and signs and symptoms of stroke are absent in VN, and if present diagnoses other than VN, such as Ménière’s disease, herpes zoster infection, infarction of the cerebellum, and brainstem should be considered.
Tests helpful in diagnosing VN include head impulse test, bi-thermal caloric test, and vestibular-evoked myogenic potential test. The head impulse test (sensitivity ranges from 0% to 100% with median sensitivity 41%% and specificity ranged between 56% and 100% (median 94%) is an easy test to perform in a primary care office. To perform this test, the patient in a seated position fixed his eyes on examiner’s nose and the examiner focused his or her eyes on the patient’s eye. The examiner holds patient’s head on both sides and moves the head to the affected side and back with a small-amplitude, high-accelerated motion. Same maneuver is repeated to the other “unaffected side.” Examiner should look for corrective rapid eye movement (saccades) and if present indicates peripheral vestibular lesion. If inconclusive, referral to a subspecialist for possible bi-thermal caloric test and vestibular-evoked myogenic potential tests is appropriate after going through the algorithm steps as outline by Rogers and colleagues (2023) and Muncie and colleagues ,
Treatment of VN can be categorized into (a) symptomatic therapy, (b) specific drug therapy, and (c) vestibular rehabilitation. Symptomatic therapy involves supportive care, anti-emetics (ondansetron, metoclopramide), and vestibular suppressants (dimenhydrinate, meclizine, scopolamine). Specific drug therapy is controversial and includes methylprednisolone, antiviral, and vasodilator therapy. Vestibular rehabilitation therapy is geared toward improving vertigo, gaze, and postural stability and improving the quality of life. With appropriate therapeutic interventions, up to 70% of patients with VN recover completely with a recurrence rate up to 11%.
Vestibular Migraine
Vestibular migraine (VM) affects 1% to 2.7% of the population and is the most common cause of non-positional vertigo. Patients diagnosed with VM have recurrent episodes of moderate to severe vestibular symptoms associated with photophobia, phonophobia, visual aura, with or without migraine like headaches. , In 2012, the International Classification of Headache Disorders and the International Classification of Vestibular Disorder Barany Society created criteria for the classification of VM which help aid in the diagnosis since there is no gold standard diagnostic testing. It may be difficult to diagnose VM from other vestibular disorders, especially in its chronic form. Diagnostic criteria for VM are listed in Box 1 . , If diagnosis is unclear, performing audiometry and/or vestibular testing should be considered to help rule out Ménière’s disease, benign positional vertigo, and other causes. An MRI of the brain may be indicated if tansient ischemic attack (TIA) or stroke is suspected.
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