Recovery from vestibular neuritis and labyrinthitis depends primarily on central compensation — the brain’s ability to recalibrate balance processing after vestibular nerve injury. Understanding what supports this compensation, and why some patients have stalled recovery, clarifies the comprehensive approach to getting back to normal function.
The acute phase of vestibular neuritis or labyrinthitis is dramatic — severe spinning vertigo, nausea, vomiting, inability to maintain upright posture, often requiring emergency evaluation and several days to a week of substantial disability. For most patients, the acute phase gradually resolves over the following days to weeks. The vestibular nerve inflammation subsides, the inner ear function partially recovers, and the brain begins the process of adapting to whatever vestibular function remains. By weeks to months after the acute event, most patients have substantially recovered, with normal or near-normal balance function restored.
Recovery from these conditions is not, however, simply a matter of the inflammation resolving. The vestibular nerve injury that produced the acute event typically leaves some degree of permanent or long-term reduction in vestibular function on the affected side. The way patients recover normal balance is through central compensation — a process by which the brain recalibrates its balance processing to account for the asymmetric vestibular input. The 2015 paper by Strupp and Magnusson in Neurologic Clinics described this central compensation as the primary mechanism of recovery from acute unilateral vestibulopathy (Strupp & Magnusson, 2015). The 2013 comprehensive review by Jeong and colleagues in Seminars in Neurology established the broader framework for understanding vestibular neuritis recovery (Jeong et al., 2013).
For most patients, central compensation proceeds normally and recovery is complete or near-complete. For some patients, however, compensation stalls or remains incomplete, leaving persistent dizziness, unsteadiness, motion sensitivity, or other vestibular symptoms long after the acute event has resolved. Understanding what supports central compensation — and what can interfere with it — clarifies why some patients recover smoothly while others develop chronic vestibular insufficiency, and what comprehensive approaches can support recovery when it has stalled.
This article walks through what central compensation actually is, what factors support normal compensation, what can interfere with the process, the clinical features of stalled or incomplete recovery, the standard evidence-based interventions that support compensation, and where addressing peripheral factors including cervical proprioceptive input may be relevant for specific patient subsets with stalled recovery.
What Central Compensation Actually Is
Understanding recovery from vestibular neuritis and labyrinthitis requires understanding what central compensation is and how it works. The process is one of the most remarkable examples of central nervous system plasticity, but it depends on specific conditions to proceed normally.
The acute vestibular event creates asymmetry
Under normal conditions, the two vestibular apparatuses (one in each inner ear) send balanced baseline signals to the brain. The brain interprets this balanced input as ‘no rotation’ — the head is stationary. When the head turns, one side increases its signal while the other decreases, and the brain interprets this asymmetric input as head rotation. The system depends on the comparison between the two sides operating from a balanced baseline.
Vestibular neuritis and labyrinthitis disrupt this balance by reducing or eliminating the signal from one side. The brain, now receiving an asymmetric baseline (high signal from intact side, low signal from affected side), interprets the asymmetry as continuous rotation. This produces the severe spinning vertigo of the acute phase. The patient feels intense rotation that does not match physical reality because the brain’s normal interpretation rules are producing a wrong answer from the asymmetric input.
Three phases of compensation
Central compensation proceeds through three overlapping phases. In the acute phase (days), the brain partially suppresses the rotation perception, reducing the intense vertigo. The vestibulo-ocular reflex adjusts toward the new baseline, reducing the spontaneous nystagmus that initially produces severe visual disturbance. In the subacute phase (weeks), the brain recalibrates its interpretation of vestibular input to account for the asymmetry. The baseline tonic firing rates adjust. The motor responses are recalibrated to produce appropriate eye and body movements based on the new input pattern. In the chronic phase (months), the recalibration becomes consolidated and stable. The brain’s processing has adapted to the asymmetric input as the new normal, and balance function operates correctly even though the underlying vestibular asymmetry remains permanent.
What compensation requires
Central compensation requires several specific things to proceed normally. Accurate sensory input from the remaining intact systems is essential — the brain needs reliable visual input, accurate proprioceptive input from throughout the body, and the residual vestibular input from the affected side and intact input from the unaffected side. Active sensory experience supports the recalibration — the brain learns to interpret the new input pattern by experiencing how the inputs correlate with actual motion and position. Time is required — the neural changes underlying compensation take days to months to develop fully. The 2010 paper by Lacour and Tighilet in Restorative Neurology and Neuroscience reviewed the mechanisms underlying central vestibular compensation (Lacour & Tighilet, 2010), establishing the framework for understanding what supports and what interferes with the process.
Why compensation can produce complete recovery
When compensation proceeds normally, patients can achieve essentially complete functional recovery even with permanent vestibular nerve damage. The brain’s processing has been recalibrated to interpret the asymmetric input correctly. Balance function operates appropriately. Eye movements are coordinated. Postural control is restored. The patient feels normal, and standard clinical examination may reveal little evidence of the underlying vestibular deficit. This complete functional recovery, despite permanent peripheral damage, is the remarkable outcome that normal central compensation produces.
Standard Acute Care for Vestibular Neuritis and Labyrinthitis
Standard medical care during the acute phase establishes the foundation for recovery. Understanding what standard care involves — and what it accomplishes — clarifies the framework within which any complementary approaches would operate.
Acute medical evaluation
Patients presenting with acute severe vertigo require urgent medical evaluation. The HINTS examination (Head Impulse, Nystagmus, Test of Skew) described by Kattah and colleagues in 2009 in Stroke distinguishes peripheral vestibular causes like vestibular neuritis from central causes like posterior circulation stroke (Kattah et al., 2009). This distinction is essential — strokes presenting with vertigo can be missed if appropriate examination is not performed, and the consequences of missed stroke can be severe. Patients should not assume their acute vertigo is vestibular neuritis without appropriate medical evaluation.
Corticosteroids
Short-course corticosteroids have evidence supporting use in acute vestibular neuritis. Studies have shown that steroids can improve the recovery of vestibular function as measured by caloric testing, though whether this translates to better long-term clinical outcomes remains debated. Methylprednisolone or prednisolone are commonly used, typically started within the first three days of symptom onset. The decision to use steroids involves balancing the potential benefits against the side effects, and individual patient factors affect this decision.
Symptomatic medications
During the acute phase, vestibular suppressant medications can reduce the severity of vertigo and nausea. Meclizine, dimenhydrinate, prochlorperazine, ondansetron, and benzodiazepines are commonly used. These medications are appropriate for short-term use (typically 2-3 days) to manage acute severe symptoms. Importantly, vestibular suppressants should not be used long-term because they interfere with central compensation — the very process that produces recovery. The 2015 paper by Strupp and Magnusson explicitly recommended limiting vestibular suppressant use to the acute phase to avoid impairing compensation.
Antivirals consideration
The viral etiology of most vestibular neuritis has led to consideration of antiviral therapy. The 2004 study by Strupp and colleagues in the New England Journal of Medicine compared steroids, antivirals, and combination therapy. Steroids alone showed benefit; antivirals alone did not show additional benefit beyond placebo; combination did not exceed steroids alone. Current practice typically does not routinely include antivirals for vestibular neuritis, though individual cases may warrant consideration.
Bacterial labyrinthitis requires different management
Bacterial labyrinthitis is a serious condition requiring different management than viral vestibular neuritis. Bacterial cases typically have associated middle ear infection, fever, hearing loss, and severe symptoms, often requiring intravenous antibiotics and sometimes surgical intervention. Distinguishing bacterial from viral cases is part of the acute medical evaluation and affects the management approach substantially.
What Supports Normal Central Compensation
Beyond the acute phase, recovery depends on supporting the central compensation process. Understanding what supports compensation clarifies what patients can do to optimize their recovery.
Vestibular rehabilitation
Vestibular rehabilitation by qualified physical therapists is one of the most established interventions supporting recovery. The rehabilitation provides structured exposure to movements and positions that challenge the vestibular system, supporting the active sensory experience that compensation requires. Specific exercises target gaze stabilization (the vestibulo-ocular reflex), postural stability, and motion sensitivity. The 2016 Cochrane review by Hillier and McDonnell concluded that vestibular rehabilitation is effective for improving outcomes in unilateral peripheral vestibular dysfunction (Hillier & McDonnell, 2016). Rehabilitation should ideally begin within the first weeks after the acute event and continue until adequate recovery is achieved.
Active movement and engagement
Beyond formal rehabilitation, active movement and engagement with normal activities support compensation. The brain learns to interpret the new vestibular input pattern through experiencing how the inputs correlate with actual motion. Bed rest beyond the first few days can impair compensation because it deprives the brain of this learning experience. Patients should be encouraged to return to normal activities as soon as the acute phase has subsided enough to allow safe activity, rather than waiting until symptoms have fully resolved. The activity itself is part of what produces resolution.
Accurate visual input
Visual input is critical for compensation because the brain uses visual information to calibrate its interpretation of vestibular signals. When patients move and visual input is reliable, the brain can correlate the visual experience with the vestibular signals, learning the new interpretation rules. Conditions that compromise visual input — uncorrected refractive errors, vision problems, prolonged time in low-light environments — can slow compensation. Optimizing visual function supports the recovery process.
Accurate proprioceptive input
Proprioceptive input — particularly from the cervical region — is another essential component of the integration that produces compensation. The 2000 study by Gdowski and McCrea in Experimental Brain Research documented direct cervical proprioceptive input to vestibular nucleus neurons (Gdowski & McCrea, 2000). The 2001 study by Kulkarni and colleagues in Neurology India documented exceptionally dense muscle spindle populations in the suboccipital muscles, indicating the cervical region as one of the most proprioceptively rich areas of the body (Kulkarni et al., 2001). The brain integrates cervical proprioceptive input with vestibular and visual input during compensation, with accurate cervical input supporting normal recalibration.
Avoidance of compensation-suppressing factors
Several factors can suppress or impair compensation and should be avoided when possible. Chronic vestibular suppressant medication use beyond the acute phase impairs compensation. Severe anxiety can interfere with the normal recalibration process. Avoidance of movement and activity deprives the brain of the experience that drives recovery. Substance use including alcohol can interfere with central processing. Addressing these factors when they are present supports compensation.
Adequate time
Compensation takes time. The neural changes underlying recovery develop over weeks to months. Most patients show substantial improvement within weeks of the acute event, but full compensation may take 3-6 months. Patients who are still symptomatic at 6 weeks should not assume their recovery is complete or that they have stalled — continued improvement over the following months is common. Patience and continued engagement with rehabilitation during this period support eventual recovery.
When Compensation Stalls or Remains Incomplete
While most patients eventually achieve substantial recovery, some have stalled or incomplete compensation that leaves persistent symptoms. Understanding the clinical picture of stalled recovery and the factors that contribute to it clarifies when comprehensive evaluation matters.
Clinical features of stalled recovery
Patients with stalled or incomplete recovery typically have persistent symptoms months after the acute event. The symptoms may include persistent unsteadiness particularly with head movements, motion sensitivity (especially with visual motion in busy environments), gaze instability when reading or with rapid head movements, fatigue with activities that challenge the vestibular system, brain fog and difficulty concentrating, anxiety about activities that provoke symptoms, and reduced confidence with daily activities. The pattern reflects continued vestibular system dysfunction that the brain has not adequately compensated for.
PPPD as a complication
Some patients with stalled recovery from vestibular neuritis develop Persistent Postural-Perceptual Dizziness (PPPD) — a functional vestibular disorder where the brain’s adaptive responses to the acute event become persistent maladaptive patterns. The PPPD framework recognizes vestibular neuritis as one of the precipitating events that can trigger this chronic functional condition. Patients with apparent stalled vestibular neuritis recovery should be evaluated for PPPD, since the condition has specific treatments different from continued vestibular rehabilitation.
Factors associated with stalled recovery
Several factors are associated with stalled or incomplete recovery. Severe initial vestibular deficit makes the compensation challenge greater. Older age can slow the neural plasticity that compensation depends on. Pre-existing anxiety or vestibular sensitivity can complicate recovery. Concurrent medical conditions affecting nervous system function can impair compensation. Inadequate engagement with rehabilitation — whether because rehabilitation wasn’t provided or because patients didn’t engage adequately — can leave compensation incomplete. Concurrent trauma to head or neck adding peripheral factors can complicate the compensation process.
The role of peripheral factors
While central compensation is the primary recovery mechanism, peripheral factors can affect how well compensation proceeds. The brain depends on the quality of the sensory inputs it integrates. When peripheral factors compromise these inputs — distorted cervical proprioception from structural problems, visual problems affecting visual input, additional vestibular system issues compounding the original neuritis — compensation may be incomplete because the inputs the brain is working with are not optimal. Addressing peripheral factors, when present, can support more complete compensation.
Distinguishing stalled recovery from other diagnoses
Patients with persistent symptoms after vestibular neuritis should be evaluated for several conditions that can produce similar pictures. PPPD is a common complication as described above. Cervicogenic dizziness can develop, particularly in patients whose acute event involved trauma or who have prominent cervical features. New onset BPPV can complicate recovery (vestibular neuritis patients have increased BPPV risk). Vestibular migraine can be activated or unmasked. Comprehensive evaluation distinguishes these distinct conditions, each of which has different specific treatment approaches.
The Role of Cervical Proprioception in Compensation
Among the peripheral factors that can affect vestibular compensation, cervical proprioception has specific relevance because of its direct anatomical connection to vestibular processing. Understanding this connection clarifies why cervical structural problems can affect recovery.
Why cervical proprioception matters specifically
The cervical region — particularly the upper cervical area — is one of the most proprioceptively rich areas of the body, with dense muscle spindle populations in the suboccipital muscles and dense mechanoreceptors in the upper cervical joints. The 1994 paper by McLain in Spine documented the density of joint mechanoreceptors in cervical facet joints, particularly the upper cervical joints (McLain, 1994). This proprioceptive richness reflects the cervical region’s importance for providing the brain with information about head position relative to the body — information that is essential for vestibular processing.
The direct neural pathway
Cervical proprioceptive input does not just contribute to general somatosensory processing — it has specific direct connections to the vestibular nuclei in the brainstem. The Gdowski and McCrea 2000 documentation of these direct cervical-to-vestibular-nucleus connections established that cervical proprioceptive information is integrated directly with vestibular input at the brainstem level (Gdowski & McCrea, 2000). For compensation, this means cervical input is part of what the brain uses to recalibrate its vestibular processing.
How distorted cervical input affects compensation
When cervical proprioceptive input is distorted by structural problems — upper cervical misalignment, chronic suboccipital muscle tension, asymmetric joint position — the brain receives unreliable information from this source. The compensation process depends on integrating multiple inputs to learn the new interpretation rules. When one of the inputs is unreliable, the integration produces less accurate results, and compensation may be less complete than it would be with accurate input. The 2003 study by Treleaven and colleagues in the Journal of Rehabilitation Medicine documented measurable cervical joint position error in patients with whiplash and dizziness (Treleaven et al., 2003), illustrating how cervical structural problems can produce measurable proprioceptive dysfunction.
Particularly relevant for dual-injury patients
Cervical proprioceptive factors are particularly relevant when vestibular neuritis or labyrinthitis occurred in the context of trauma — for example, a patient who was in a motor vehicle accident and subsequently developed vestibular nerve dysfunction. The 2005 study by Kaale and colleagues in the Journal of Neurotrauma documented upper cervical ligamentous injuries from whiplash mechanisms at forces below those required for diagnosable concussion (Kaale et al., 2005). When trauma was sufficient to affect vestibular function, the upper cervical structures essentially always experienced forces above the threshold for their own injury. For these dual-injury patients, the cervical structural problems can contribute to ongoing distorted proprioceptive input affecting compensation.
The 2022 comprehensive review
The 2022 paper by Peng and colleagues in the Journal of Clinical Medicine provided the comprehensive narrative review of proprioceptive cervicogenic dizziness, including the framework for understanding how cervical proprioceptive dysfunction can affect balance processing (Peng et al., 2022). The review establishes the cervical proprioceptive contribution as recognized in mainstream vestibular medicine, though specifically as one component of cervicogenic dizziness rather than as a primary cause of typical vestibular neuritis.
Where Upper Cervical Evaluation May Support Recovery
For specific patient subsets with stalled or incomplete recovery, upper cervical evaluation may be one component of comprehensive care. The relevance is most clear for patients with dual-injury circumstances or prominent cervical features.
Stalled recovery with prior trauma
Patients whose vestibular neuritis occurred in the context of head or neck trauma — particularly when the trauma was significant — and who have stalled recovery represent the clearest case for upper cervical evaluation. The dual injury reality means cervical structural problems are essentially always present, and the cervical contribution to ongoing distorted proprioceptive input may be impairing compensation. Addressing the cervical structural component can support more complete recovery alongside continued vestibular rehabilitation.
Persistent cervical symptoms alongside vestibular symptoms
Patients whose stalled vestibular recovery is accompanied by prominent cervical symptoms — chronic neck pain, suboccipital tension, restricted cervical range of motion, cervicogenic headache patterns — may have substantial cervical structural involvement that is contributing to the broader picture. The cervical evaluation addresses one specific component, with continued vestibular rehabilitation addressing the central compensation aspect.
Treatment-resistant stalled recovery
Patients whose recovery has not progressed despite adequate vestibular rehabilitation, time, and other appropriate measures may benefit from evaluation of factors that standard treatment does not specifically address. Upper cervical structural problems can be one such factor. Adding cervical evaluation to continued comprehensive care can be reasonable for these treatment-resistant cases, particularly when other features suggest cervical involvement.
When upper cervical evaluation is NOT indicated
Many vestibular neuritis and labyrinthitis patients do not particularly need upper cervical evaluation. Patients in the acute phase need medical care, not chiropractic intervention. Patients in the early recovery phase (first weeks) should focus on rehabilitation rather than additional interventions. Patients with smooth recovery progress do not need additional approaches. Patients with classic viral vestibular neuritis without trauma and without cervical features have minimal cervical involvement and should focus on standard recovery support. For these patients, focusing fully on vestibular rehabilitation and time is appropriate.
How the evaluation works for appropriate patients
For appropriate patients, upper cervical chiropractic uses three-dimensional cone beam CT imaging to measure alignment with precision, objective testing (leg length analysis, paraspinal thermography) before any intervention, and specific low-force corrections rather than aggressive manipulation. The precision is particularly important for patients still recovering from vestibular events whose systems may be sensitized — aggressive cervical manipulation could potentially aggravate the vestibular symptoms and is not appropriate. When correction provides benefit, it supports compensation rather than replacing it. The vestibular rehabilitation continues and may become more effective when the cervical proprioceptive input contributing to compensation has been improved.
Honest evidence framing
Patients should understand that no randomized controlled trials demonstrate upper cervical chiropractic as effective intervention for supporting vestibular neuritis recovery specifically. The reasoning supporting cervical evaluation for patients with stalled recovery and dual-injury circumstances is anatomically grounded in the established mechanisms of cervical contribution to balance processing, but the trial-level evidence specific to upper cervical care for this purpose is limited. The intervention should be approached as a complementary consideration based on anatomical reasoning for appropriate patient subsets, not as established standard care.
When to Consider Comprehensive Evaluation for Stalled Recovery
If you are recovering from vestibular neuritis or labyrinthitis and your recovery seems to have stalled, several considerations matter for next steps.
First, ensure adequate vestibular rehabilitation. Many patients are not provided with formal vestibular rehabilitation or do not receive enough rehabilitation. If you have not had several months of vestibular rehabilitation with a qualified physical therapist, this should be your first priority. Standard rehabilitation often produces substantial improvement even months after the acute event.
Second, evaluate for PPPD or other complications. Persistent symptoms after vestibular neuritis may represent PPPD development rather than simply continued vestibular deficit. PPPD has specific treatments different from continued rehabilitation. Otolaryngology or neurology evaluation can establish whether PPPD or another condition has developed.
Third, consider whether comprehensive evaluation including upper cervical assessment may be appropriate if any of the following are true: Your vestibular neuritis occurred in the context of head or neck trauma. You have persistent cervical symptoms alongside your vestibular symptoms. Your recovery has stalled despite adequate vestibular rehabilitation. You have features of cervicogenic dizziness mixed with your stalled vestibular neuritis recovery. You have prior concussions or significant neck trauma layered on the current presentation.
For patients with classic viral vestibular neuritis without trauma, smooth recovery progress, no cervical features, or recent acute events still in normal recovery timeline, focusing on standard rehabilitation and time is appropriate. Not every patient with stalled recovery needs cervical evaluation — the cervical angle is most relevant for specific subsets.
To find an upper cervical chiropractor near you, visit www.neckwise.com.
Where to Go From Here
Recovery from vestibular neuritis and labyrinthitis depends primarily on central compensation — the brain’s ability to recalibrate balance processing after vestibular nerve injury. The process requires accurate sensory inputs from visual, vestibular, and proprioceptive sources; active movement and engagement; vestibular rehabilitation when provided; and adequate time. For most patients, compensation proceeds normally and produces substantial recovery. For some patients, compensation stalls or remains incomplete, leaving persistent symptoms months after the acute event.
Comprehensive support for compensation involves vestibular rehabilitation as the foundation, addressing factors that can interfere with the normal process, and evaluating for complications like PPPD that may explain persistent symptoms. For specific patient subsets — particularly those whose vestibular event occurred with concurrent trauma, those with persistent cervical symptoms alongside stalled recovery, and those with treatment-resistant patterns — upper cervical evaluation can be one component of comprehensive care. The cervical proprioceptive input is part of what the brain uses for compensation, and addressing structural cervical problems may support more complete recovery in appropriate patients. The evaluation should be approached as a complementary consideration alongside continued standard care, with realistic expectations and continued engagement with vestibular rehabilitation.
For patients in the acute phase or early recovery, medical evaluation and vestibular rehabilitation form the foundation of care. For patients with stalled recovery, comprehensive evaluation including assessment for PPPD, cervicogenic factors, and other complications may clarify next steps. The path to recovery is supported by understanding the central compensation process and what helps it proceed normally.
To find an upper cervical chiropractor near you, visit www.neckwise.com.
References
- Strupp, M., & Magnusson, M. (2015). Acute unilateral vestibulopathy. Neurologic Clinics, 33(3), 669–685.
- Jeong, S. H., Kim, H. J., & Kim, J. S. (2013). Vestibular neuritis. Seminars in Neurology, 33(3), 185–194.
- Strupp, M., Zingler, V. C., Arbusow, V., et al. (2004). Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. New England Journal of Medicine, 351(4), 354–361.
- Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome. Stroke, 40(11), 3504–3510.
- Hillier, S. L., & McDonnell, M. (2016). Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database of Systematic Reviews, (1), CD005397.
- Lacour, M., & Tighilet, B. (2010). Plastic events in the vestibular nuclei during vestibular compensation: The brain orchestration of a ‘deafferentation’ code. Restorative Neurology and Neuroscience, 28(1), 19–35.
- Gdowski, G. T., & McCrea, R. A. (2000). Neck proprioceptive inputs to primate vestibular nucleus neurons. Experimental Brain Research, 135(4), 511–526.
- Kulkarni, V., Chandy, M. J., & Babu, K. S. (2001). Quantitative study of muscle spindles in suboccipital muscles of human foetuses. Neurology India, 49(4), 355–359.
- McLain, R. F. (1994). Mechanoreceptor endings in human cervical facet joints. Spine, 19(5), 495–501.
- Treleaven, J., Jull, G., & Sterling, M. (2003). Dizziness and unsteadiness following whiplash injury: Characteristic features and relationship with cervical joint position error. Journal of Rehabilitation Medicine, 35(1), 36–43.
- Peng, B., Yang, L., Yang, C., Pang, X., Chen, X., & Wu, Y. (2022). Proprioceptive cervicogenic dizziness: A narrative review of pathogenesis, diagnosis, and treatment. Journal of Clinical Medicine, 11(21), 6293.
- Kaale, B. R., Krakenes, J., Albrektsen, G., & Wester, K. (2005). Head position and impact direction in whiplash injuries: Associations with MRI-verified lesions of ligaments and membranes in the upper cervical spine. Journal of Neurotrauma, 22(11), 1294–1302.
This article is educational in nature and does not constitute medical advice, diagnosis, or treatment. Individual results vary. Chiropractic care focuses on the structure and function of the spine and nervous system. Patients with vestibular neuritis, labyrinthitis, or related conditions should pursue appropriate medical evaluation by otolaryngology, neurology, or other appropriate specialists and engage with evidence-based standard treatments including vestibular rehabilitation as the foundation of care. Upper cervical evaluation should be considered only for specific patient subsets as a complementary approach rather than a primary treatment. Patients with acute severe vertigo, new neurological symptoms, sudden hearing loss, or other red flag features should seek urgent medical evaluation. No claim is made or implied that upper cervical chiropractic cures or treats vestibular neuritis, labyrinthitis, or any other specific disease.