Disclaimer: This information is intended for educational purposes only and does not constitute medical advice. It is designed to supplement, not replace, the clinical judgment of healthcare professionals. Patient care decisions must be based on the individual circumstances of each patient, current medical knowledge, and the clinician's experience. Always consult with a qualified healthcare provider for diagnosis and treatment of any medical condition.

Vestibular Neuritis

Overview

• Definition: Vestibular neuritis (VN) is an acute, spontaneous, and usually single-episode peripheral vestibulopathy characterized by the sudden onset of severe vertigo, nausea, vomiting, and gait instability, without associated auditory (tinnitus, hearing loss) or focal neurological symptoms. It results from inflammation of the vestibular nerve, typically unilateral. It is also sometimes referred to as "vestibular neuronitis" or, less commonly, "labyrinthitis" (if hearing loss is present, it's typically viral labyrinthitis, involving the cochlea as well).
• Epidemiology: VN is one of the most common causes of acute prolonged vertigo, accounting for up to 15% of patients presenting with dizziness.
  • Incidence: Estimated at 3.5 to 15 cases per 100,000 population per year.
  • Demographics: Affects adults of all ages, but is most common in individuals aged 30 to 60 years. There is no significant gender predominance.
  • Seasonality: Some studies suggest a higher incidence in spring and early summer, correlating with viral infection patterns.
• Classification:
  • Classical Vestibular Neuritis: Involves inflammation primarily of the superior division of the vestibular nerve, affecting the anterior and horizontal semicircular canals and utricle. This is the most common presentation.
  • Inferior Vestibular Neuritis: Less common, involves the inferior division of the vestibular nerve, affecting the posterior semicircular canal and saccule. Patients may present with isolated benign paroxysmal positional vertigo (BPPV) of the posterior canal as a sequela due to damage to the saccule and posterior canal afferents.
  • Recurrent Vestibular Neuritis: While VN is typically a single episode, recurrent forms have been reported, though they are much less common and prompt consideration of alternative diagnoses such as vestibular migraine, Meniere's disease, or even autoimmune inner ear disease.

Pathophysiology

• Mechanism: The exact mechanism is not fully understood, but the prevailing theory is that VN is caused by a viral infection leading to inflammation of the vestibular nerve.
  • Viral Etiology: Herpes Simplex Virus type 1 (HSV-1) is the most commonly implicated pathogen, supported by serological studies and reactivation patterns. Other viruses, such as Epstein-Barr Virus, cytomegalovirus, influenza, and adenovirus, have also been suggested. The virus is thought to reactivate from the vestibular ganglia (similar to herpes zoster causing Ramsay Hunt syndrome) or cause a direct inflammatory response.
  • Inflammation: The inflammation leads to demyelination or neuronal damage, causing a sudden unilateral vestibular hypofunction. This creates an acute imbalance in tonic neural activity between the two vestibular nuclei, leading to the sensation of vertigo.
  • Vascular Etiology: Less commonly, microvascular ischemia of the vestibular nerve or labyrinthine artery has been proposed as a potential cause, particularly in older patients with vascular risk factors.
• Risk Factors:
  • Recent Viral Infection: A history of recent upper respiratory tract infection, gastrointestinal illness, or flu-like symptoms often precedes the onset of VN.
  • Stress: While not a direct cause, psychological stress may act as a trigger for viral reactivation.
  • Immunocompromised State: Potentially increases susceptibility to viral reactivation, though VN can occur in healthy individuals.
  • Genetic Predisposition: No strong genetic link has been identified, but individual susceptibility to viral infections may play a role.
• Protective Factors: No specific protective factors for vestibular neuritis are known. General health maintenance, vaccination against common viral illnesses (e.g., influenza), and a healthy immune system may indirectly contribute, but do not prevent the condition.

Clinical Presentation

Signs and Symptoms

• Cardinal Features:
  • Acute onset, severe rotational vertigo: The hallmark symptom, often described as a spinning sensation, disequilibrium, or feeling of being pulled to one side. It is constant and worsened by head movements.
  • Nausea and vomiting: Common and often severe due to the intense vestibular stimulation.
  • Gait instability: Patients typically struggle to walk without support and often veer towards the affected side. They may be unable to stand or walk without falling.
  • Absence of auditory symptoms: Crucially, there is no hearing loss or tinnitus, which helps differentiate VN from Meniere's disease or labyrinthitis.
  • Absence of focal neurological deficits: No weakness, numbness, diplopia, dysarthria, or other signs indicative of central nervous system involvement.
• Early Signs:
  • Sudden, unprovoked onset of vertigo that reaches its peak intensity within hours (typically 24-48 hours).
  • Significant nausea and vomiting often leading to dehydration.
  • Profound difficulty with ambulation.
• Advanced Signs:
  • After the acute phase (days to weeks), the severe vertigo gradually subsides, but patients may experience persistent mild dizziness, disequilibrium, and sensitivity to head movements.
  • Oculomotor disturbances: Persistent spontaneous nystagmus (though less intense), or positional nystagmus.
  • Visual blurring (oscillopsia): Especially during head movements, due to impaired vestibulo-ocular reflex (VOR).
• Atypical Presentations:
  • Mild symptoms: While usually severe, some cases may present with less intense vertigo, making diagnosis challenging.
  • Recurrent episodes: While rare for true VN, recurrent vertigo should prompt consideration of alternative diagnoses (e.g., vestibular migraine, Meniere's disease, or a "compensated" VN that recurs due to another cause).
  • Late onset BPPV: As a sequela of inferior vestibular neuritis, patients may develop BPPV due to otoconial detachment.

Physical Examination

The physical examination is crucial for differentiating peripheral vertigo (like VN) from central causes, especially in the acute setting. - Inspection: * Spontaneous Nystagmus: A key finding. In acute VN, there is a spontaneous, unidirectional, horizontal-rotatory nystagmus that beats away from the lesioned side (i.e., towards the healthy ear). This nystagmus is typically inhibited by visual fixation and enhanced by removing visual fixation (e.g., using Frenzel lenses or looking in the dark). * Head Position: Patients often prefer to lie still with their head fixed, as any head movement exacerbates vertigo. - Palpation: Not directly relevant for diagnosis of VN. - Special Tests: The HINTS exam (Head Impulse, Nystagmus, Test of Skew) is critical for distinguishing peripheral from central causes of acute vestibular syndrome. * Head Impulse Test (HIT): Also known as the Head Impulse Test (or Halmagyi-Curthoys test). This is the most sensitive bedside test for detecting peripheral vestibular hypofunction. * Procedure: The examiner rapidly turns the patient's head approximately 10-20 degrees to one side while the patient fixes their gaze on the examiner's nose. * Finding in VN (Peripheral Lesion): A positive HIT (corrective saccade) occurs when the patient's eyes move off the target and then make a rapid "catch-up" saccade back to the target after the head movement, indicating impaired VOR on the side to which the head is turned. If the head is turned quickly to the right and the eyes drift right and then saccade back left, it indicates a right-sided vestibular deficit. * Nystagmus (Spontaneous/Gaze-evoked): * Finding in VN (Peripheral Lesion): Unidirectional, horizontal-rotatory nystagmus that does not change direction with gaze (e.g., always beats to the right, regardless of whether the patient looks right or left). It is suppressed by visual fixation. * Contrast to Central Nystagmus: Central nystagmus can be purely vertical, purely torsional, bidirectional (changes direction with gaze), or persistent with visual fixation. * Test of Skew (Cover-Uncover Test): * Procedure: Cover one eye for a few seconds, then uncover it and observe for vertical refixation of the eye. Repeat for the other eye. * Finding in VN (Peripheral Lesion): Absence of skew deviation (no vertical misalignment of the eyes). * Contrast to Central Lesion: The presence of skew deviation strongly suggests a central lesion (e.g., brainstem or cerebellar stroke). * HINTS Plus: Add "Plus" to the HINTS exam if there's hearing loss. If a patient has acute vestibular syndrome, a positive HINTS test AND unilateral hearing loss suggests an anterior inferior cerebellar artery (AICA) stroke rather than a peripheral disorder. * Romberg Test: Patients with VN will typically fall towards the affected side. * Gait Assessment: Patients typically exhibit a wide-based gait and tend to fall or veer towards the affected side, especially with eyes closed or in the dark. * Caloric Testing: If performed (usually by a specialist after the acute phase), it typically shows unilateral caloric paresis (reduced or absent response) on the affected side, consistent with vestibular hypofunction.

Diagnostic Approach

History Taking

• Key Questions:
  • Onset: Was the onset sudden? How rapidly did symptoms peak?
  • Nature of Dizziness: Is it true spinning vertigo or just lightheadedness/imbalance?
  • Associated Symptoms:
    • Auditory: Any hearing loss, tinnitus, ear fullness? (Absence suggests VN).
    • Neurological: Headache, double vision, slurred speech, weakness, numbness, difficulty swallowing, change in consciousness? (Presence suggests central cause).
    • Systemic: Nausea, vomiting, fever, recent illness (URI, GI)?
  • Exacerbating/Alleviating Factors: What makes it worse (e.g., head movement, sitting up, standing)? What makes it better (e.g., lying still)?
  • Past Medical History: Previous episodes of dizziness, migraines, cardiovascular disease, risk factors for stroke (hypertension, diabetes, hyperlipidemia, smoking), autoimmune conditions.
  • Medications: Current medications, especially ototoxic drugs.
• Red Flags: These suggest a central (brainstem/cerebellar) lesion, requiring urgent neuroimaging.
  • "Infirm" HINTS Exam:
    • Negative Head Impulse Test: VOR intact, eyes stay on target despite rapid head turns.
    • Direction-changing Nystagmus with Gaze: Nystagmus that beats right when looking right, and left when looking left.
    • Skew Deviation (Cover-Uncover test is positive): Vertical ocular misalignment.
  • Isolated new headache or severe headache: Especially if sudden onset "thunderclap."
  • Focal neurological deficits: Diplopia, dysarthria, dysphagia, facial droop, limb weakness, numbness, sensory loss.
  • Ataxia disproportionate to vertigo: Patient cannot sit or stand without support, even when vertigo is not extreme.
  • Altered consciousness or severe drowsiness.
  • New-onset seizure.
  • Risk factors for stroke (especially in older patients).

Laboratory Tests

• First-Line:
  • Generally not indicated for the diagnosis of typical vestibular neuritis, which is a clinical diagnosis.
  • If systemic illness is suspected (e.g., severe vomiting, dehydration), basic labs like electrolytes and renal function might be considered.
• Confirmatory: No specific laboratory test confirms vestibular neuritis.
• Monitoring: No specific lab tests for monitoring VN recovery.

Imaging

• Recommended:
  • Brain imaging (MRI with diffusion-weighted imaging (DWI)) is NOT routinely recommended for typical presentations of vestibular neuritis.
  • MRI is crucial for excluding central pathology (e.g., stroke, demyelinating disease, tumor) when red flags are present, or when the HINTS exam is "infirm."
• Advanced:
  • MRI of the brain with gadolinium: Should be performed urgently if a central cause is suspected based on history or physical exam (especially an "infirm" HINTS). MRI can visualize brainstem or cerebellar lesions, and rarely, inflammation of the vestibular nerve itself.
  • CT scan of the head: Less useful than MRI for acute stroke in the posterior fossa but may be used in emergency settings to rule out hemorrhage if MRI is unavailable.

Management

Acute Management

The primary goals in the acute phase are symptom relief and prevention of complications. - Immediate (within first 24-48 hours): * Symptomatic Relief: * Antiemetics: To control nausea and vomiting. Examples: * Ondansetron: 4-8 mg IV/PO every 4-8 hours as needed. * Promethazine: 12.5-25 mg IV/IM/PO every 4-6 hours as needed. * Prochlorperazine: 5-10 mg IV/IM/PO every 6 hours as needed. * Vestibular Suppressants: To reduce vertigo and nystagmus. These should be used for the shortest possible duration (typically no more than 2-3 days) to avoid hindering central compensation. * Antihistamines (first-generation): Sedating effects may be beneficial. * Meclizine: 25-50 mg PO every 6-8 hours as needed. * Dimenhydrinate: 50 mg PO/IM/IV every 4-6 hours as needed. * Benzodiazepines: Use with caution due to sedation and risk of dependence. * Diazepam: 2-5 mg PO/IV every 6-8 hours as needed. * Lorazepam: 0.5-1 mg PO/IV every 6-8 hours as needed. * Hydration: IV fluids may be necessary if vomiting is severe. - Stabilization (within 72 hours of onset): * Corticosteroids: The use of corticosteroids for vestibular neuritis is debated but often considered, particularly if initiated within 72 hours of symptom onset. The rationale is to reduce inflammation of the vestibular nerve. * Regimen: Prednisone: Typically 60 mg orally once daily for 5 days, followed by a taper over 5-10 days (e.g., decrease by 10 mg/day or half the dose every 2 days). * Evidence: A Cochrane review suggests a possible benefit in long-term vestibular function recovery, but the clinical impact on vertigo severity and duration is less clear. Early initiation appears crucial. - Emergency: If red flags for a central cause are present (e.g., "infirm" HINTS, new neurological deficit), immediate emergency evaluation, including urgent neuroimaging (MRI brain with DWI), is paramount to rule out stroke or other life-threatening conditions.

Chronic Management

The focus shifts from symptom suppression to promoting central vestibular compensation. - Pharmacological: * Vestibular Suppressants: DISCONTINUE vestibular suppressants as soon as acute symptoms subside (ideally within 48-72 hours). Prolonged use hinders the brain's natural process of compensation, leading to chronic dizziness. * Antidepressants/Anxiolytics: If patients develop persistent anxiety, depression, or a functional vestibular disorder like Persistent Postural-Perceptual Dizziness (PPPD) as a sequela, SSRIs (e.g., sertraline, escitalopram) or SNRIs (e.g., venlafaxine) may be beneficial. - Non-pharmacological: * Vestibular Rehabilitation Therapy (VRT): This is the cornerstone of chronic management and is crucial for promoting central compensation. VRT involves specific exercises designed to: * Gaze Stabilization Exercises: To improve VOR (e.g., looking at a target while moving the head). * Habituation Exercises: To reduce dizziness by repeatedly exposing the patient to movements that provoke symptoms. * Balance Training: To improve postural stability and gait (e.g., tandem walking, walking on uneven surfaces). * Activity and Exercise: Encouraging early mobilization and return to normal activities helps the brain adapt. * Lifestyle Modifications: Avoiding triggers for dizziness (e.g., sudden head movements in early recovery), maintaining good hydration, and managing stress. * Psychological Support: Cognitive behavioral therapy (CBT) can be helpful for patients developing anxiety, phobia, or PPPD related to their dizziness. - Monitoring: * Regular follow-up with the primary care physician or a specialist (e.g., neurotologist, neurologist, physical therapist) to assess recovery, monitor for persistent symptoms, and adjust the VRT program. * Assessment of functional status and quality of life.

Treatment Algorithms

• First-Line:
  1. Exclude central causes: Perform thorough history and HINTS exam. If red flags, obtain urgent MRI.
  2. Symptomatic control: Short course (2-3 days maximum) of antiemetics and vestibular suppressants.
  3. Corticosteroids: Consider a short course of oral prednisone (e.g., 60 mg daily for 5 days then taper over 5-10 days) if presenting within 72 hours.
  4. Early Mobilization: Encourage ambulation and head movements as tolerated.
  5. Referral for Vestibular Rehabilitation Therapy (VRT): Initiate VRT as soon as acute nausea/vomiting subsides, usually within days of onset.
• Second-Line:
  1. Persistent dizziness/imbalance: Aggressive VRT, possibly with a specialized vestibular therapist.
  2. Development of BPPV: Treat with appropriate repositioning maneuvers (e.g., Epley maneuver for posterior canal BPPV).
• Refractory Cases:
  1. Re-evaluate diagnosis: If symptoms persist beyond 3-6 months despite adequate VRT, re-evaluate for alternative or comorbid diagnoses (e.g., vestibular migraine, PPPD, malingering, unrecognized central lesion).
  2. Specialist referral: Refer to a neurotologist, neurologist, or specialized dizziness clinic for further diagnostic workup (e.g., advanced vestibular testing like vHIT, VEMPs) and management.
  3. Pharmacological for secondary conditions: Consider SSRIs/SNRIs for PPPD or comorbid anxiety/depression.

Complications

• Common:
  • Persistent Imbalance/Dizziness: Even after the acute vertigo resolves, many patients experience residual disequilibrium, especially with quick head movements or in visually complex environments. This indicates incomplete central compensation.
  • Anxiety and Depression: The acute, disabling nature of vertigo and fear of recurrence can lead to significant psychological distress.
  • Benign Paroxysmal Positional Vertigo (BPPV): Especially posterior canal BPPV, which can occur as a sequela of inferior vestibular neuritis due to otoconial detachment.
• Serious:
  • Chronic Vestibular Dysfunction: A minority of patients (5-15%) fail to compensate adequately, leading to chronic disability, impaired quality of life, and increased risk of falls.
  • Persistent Postural-Perceptual Dizziness (PPPD): A functional disorder characterized by chronic non-spinning dizziness, unsteadiness, or rocking sensation worsened by upright posture, self-motion, or visual stimuli. It often develops after an acute vestibular event like VN.
  • Falls and Injuries: Due to severe imbalance, especially in older adults.
• Long-term:
  • Reduced vestibulo-ocular reflex (VOR) gain on the affected side, demonstrable with caloric testing or video head impulse test (vHIT).
  • Social isolation and reduced activity levels due to fear of dizziness.

Prognosis

• Factors:
  • Age: Younger patients tend to compensate more effectively than older adults.
  • Severity of Initial Attack: More severe initial symptoms may correlate with slower recovery.
  • Early Initiation of VRT: Crucial for optimal recovery. Delay or absence of VRT can lead to poorer outcomes.
  • Comorbidities: Pre-existing anxiety, depression, other neurological conditions, or cardiovascular disease can hinder recovery.
  • Psychological Factors: Fear avoidance behavior, kinesiophobia can impede compensation.
• Survival: Excellent prognosis for life; vestibular neuritis is not a life-threatening condition.
• Morbidity:
  • Most patients (around 70-85%) recover well with significant reduction or resolution of symptoms within weeks to a few months.
  • However, up to 15-30% may experience chronic, persistent symptoms (e.g., disequilibrium, motion sensitivity, PPPD) that can significantly impact quality of life.
• Quality of Life: Can be severely impacted in the acute phase. With successful compensation, most patients return to their baseline activities. For those with chronic symptoms, quality of life may remain impaired without appropriate management (e.g., VRT, psychological support).

Prevention

• Primary:
  • No specific primary prevention strategies for vestibular neuritis.
  • General health maintenance and vaccination against common viral illnesses (e.g., influenza, varicella) may offer some indirect protection, but specific prevention against HSV-1 (the most common implicated virus) is not practical for this condition.
• Secondary:
  • Early Diagnosis: Prompt and accurate diagnosis of vestibular neuritis is crucial to differentiate it from central causes and initiate appropriate management.
  • Early Vestibular Rehabilitation Therapy (VRT): Initiating VRT as soon as possible after the acute phase (once nausea/vomiting improve) can significantly improve outcomes and prevent chronic dizziness by promoting central compensation. Avoiding prolonged use of vestibular suppressants is also a key secondary prevention strategy for chronic symptoms.
• Tertiary:
  • Management of Complications: Aggressive treatment of BPPV if it develops (repositioning maneuvers).
  • Treatment of PPPD: If chronic non-rotational dizziness develops, a combination of VRT, cognitive behavioral therapy (CBT), and sometimes medication (SSRIs/SNRIs) can help manage PPPD and improve quality of life.
  • Psychological Support: Addressing anxiety and depression early can prevent them from becoming chronic barriers to recovery.

Special Populations

• Pediatric:
  • Vestibular neuritis is rare in children but can occur. Diagnosis can be challenging as children may have difficulty verbalizing symptoms.
  • The presentation may be less dramatic, but acute onset vertigo, nystagmus, and gait disturbance are still key features.
  • Exclusion of central causes remains paramount. Treatment principles are similar, with emphasis on VRT, but medication dosages need careful adjustment.
• Geriatric:
  • Older adults are at higher risk for falls due to vestibular dysfunction, comorbidities, and polypharmacy.
  • Compensation may be slower and less complete compared to younger adults due to age-related decline in central processing and brain plasticity.
  • Comorbidities (e.g., cardiovascular disease, diabetes, neurological conditions) can complicate diagnosis and management. Stroke risk is higher, making the HINTS exam even more critical.
  • Careful consideration of medication side effects (e.g., sedation from vestibular suppressants, benzodiazepines) which can increase fall risk. VRT is essential but may need to be adapted for physical limitations.
• Pregnancy:
  • Management of acute vertigo in pregnancy requires careful consideration of medication safety.
  • Antiemetics like ondansetron are generally considered safe. First-generation antihistamines (e.g., meclizine) can also be used cautiously. Benzodiazepines are generally avoided, especially in the first trimester.
  • Corticosteroids are typically avoided unless the benefit clearly outweighs the risk, especially in the first trimester. Consult with an obstetrician.
  • VRT is safe and should be encouraged.
• Comorbidities:
  • Migraine: Differentiating vestibular neuritis from vestibular migraine can be challenging, especially in patients with a history of migraine. VN is typically a single acute event, whereas vestibular migraine can be recurrent. Co-occurrence is possible, and VN may trigger subsequent vestibular migraine episodes.
  • Anxiety Disorders/Depression: Pre-existing anxiety or depression can exacerbate the perception of dizziness and hinder vestibular compensation. Management should include addressing these underlying conditions, often with psychotherapy and/or appropriate pharmacotherapy (SSRIs/SNRIs).
  • Cardiovascular Disease: Increased stroke risk requires heightened vigilance for central causes. Blood pressure and glucose control are important general health measures.

Clinical Pearls

• Diagnostic:
  • HINTS Exam is your best friend: In the setting of acute vestibular syndrome, a "positive" HINTS exam (unidirectional nystagmus, positive head impulse test, no skew deviation) strongly indicates a peripheral lesion (like VN). An "infirm" HINTS (negative head impulse test, direction-changing nystagmus, skew deviation) should immediately raise suspicion for a central lesion (e.g., stroke) and prompt urgent neuroimaging.
  • Absence of auditory symptoms (hearing loss or tinnitus) is a key differentiator from labyrinthitis or Meniere's disease.
  • Vertigo is constant for days, not episodic, unlike BPPV or Meniere's. It is worsened by head movement but is not only triggered by position changes.
• Treatment:
  • Less is More with Vestibular Suppressants: Use for shortest possible duration (2-3 days max) to prevent hindering central compensation. Early discontinuation is crucial for recovery.
  • Early Mobilization and Vestibular Rehabilitation are Key: Encourage patients to get up and move as soon as possible after the acute nausea subsides. Referral to a vestibular therapist for VRT is highly recommended and promotes long-term recovery.
  • Consider Steroids Early: If used, start prednisone within 72 hours of symptom onset for potential benefit in vestibular function recovery.
• Pitfalls:
  • Missing a Central Cause: The most dangerous pitfall. Always perform a thorough neurological exam and HINTS in acute vertigo. Do not rely solely on patient report.
  • Prolonged Use of Vestibular Suppressants: This is a common mistake that delays recovery and can lead to chronic dizziness.
  • Ignoring Psychological Impact: Failure to address anxiety, depression, or fear-avoidance behaviors can lead to persistent functional disability, even if the vestibular system has compensated.
  • Inadequate VRT: Patients need specific, tailored exercises, not just general advice to "move around."

Recent Updates

• Guidelines: The American Academy of Neurology (AAN) published a guideline on acute dizziness and vertigo in 2013, which emphasizes the utility of the HINTS exam in the acute vestibular syndrome. While specific guidelines on steroid use are still debated, the trend remains towards considering early use. The Bárány Society has developed diagnostic criteria for various vestibular disorders, including Vestibular Neuritis.
• Evidence:
  • Continued research supports the efficacy of vestibular rehabilitation therapy (VRT) as the cornerstone of recovery for vestibular neuritis, significantly improving long-term outcomes and reducing chronic dizziness.
  • The role of corticosteroids remains controversial, with some studies showing a modest benefit in vestibular function recovery (e.g., caloric test normalization) when given early (within 3 days), but less clear benefit on symptom resolution or overall recovery time. Anti-viral therapy has generally not shown significant benefit.
  • Increasing recognition of Persistent Postural-Perceptual Dizziness (PPPD) as a common sequela of acute vestibular events like VN, highlighting the importance of psychological and rehabilitative interventions for chronic symptoms.
• Controversies:
  • Optimal Steroid Regimen: The ideal dose, duration, and patient selection for corticosteroid treatment remain subjects of debate.
  • Role of Antivirals: Despite the presumed viral etiology, antiviral medications have not consistently demonstrated benefit in clinical trials for VN.
  • Predictors of Non-recovery: Identifying specific factors that predict poor recovery and progression to chronic dizziness is an ongoing area of research.

Key References

• Guidelines:
  • Kattah, J. C., et al. "HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging." Stroke, 2009. (Landmark paper for HINTS exam)
  • Neuhauser, H. K., & Lempert, T. "Vertigo and dizziness." New England Journal of Medicine, 2009.
  • Strupp, M., et al. "Pharmacotherapy of vestibular disorders." Journal of Neurology, 2011. (Review of medical treatments for vestibular disorders, including VN)
  • McDonnell, M. N., & O'Connell, N. E. "Vestibular rehabilitation for unilateral peripheral vestibular dysfunction." Cochrane Database of Systematic Reviews, 2009. (Evidence for VRT)
• Studies:
  • Strupp, M., et al. "Prednisone vs. valaciclovir in acute vestibular neuritis: a randomized, double-blind, placebo-controlled study." New England Journal of Medicine, 2004. (Key study on steroid and antiviral efficacy)
  • Sloane, P. D., et al. "Acute dizziness and vertigo: AAN Practice Guideline." Neurology, 2013.
• Reviews:
  • Dieterich, M., & Brandt, T. "Vestibular neuritis: new insights into a classic disorder." Journal of Neurology, Neurosurgery & Psychiatry, 2008.
  • Kim, J. S., & Zee, D. S. "Clinical Approach to Acute Vertigo." Practical Neurology, 2014.