Response – Paroxysmal Positional Vertigo (BPPV) and Meniere’s Disease (MD)

Response – Paroxysmal Positional Vertigo (BPPV) and Meniere’s Disease (MD)

Hello,

Your post compares benign paroxysmal positional vertigo (BPPV) and Meniere’s disease (MD), covering presentation, pathophysiology, assessment, diagnosis, and management. You effectively highlighted the differences in symptom duration and triggers between BPPV and MD. Notably, BPPV episodes are brief and triggered by head movements, whereas MD episodes are longer and not necessarily triggered by specific movements (Johns & Quinn, 2020). MD can significantly impact a patient’s quality of life due to its association with hearing loss and tinnitus.

Further, your explanation of the underlying mechanisms of BPPV and MD is thorough. The distinction between the calcium debris in the semicircular canals causing BPPV and the endolymphatic hydrops in MD is crucial. The idiopathic nature of many BPPV cases contrasts with the multifactorial etiology of MD. Following this, the use of the Dix-Hallpike manoeuvres for BPPV and the importance of audiometric testing for MD are well noted. Including the HINTS (head-impulse, nystagmus, test-of-skew) examination for differentiating peripheral from central causes of vertigo is valuable (Li et al., 2023). This tool can help identify serious conditions such as stroke, which can present with vertigo.

Consistently, the management strategies for both conditions are well articulated. For BPPV, the emphasis on manoeuvres such as the Epley and Semont techniques aligns with current best practices (Pauwels et al., 2023). Additionally, for MDs, combining pharmacologic treatments like antiemetics and diuretics with lifestyle modifications can help manage symptoms and improve patient outcomes. The potential need for surgical intervention in severe MD cases also highlights the complexity of managing this condition.

Conclusively, your post provides a robust and insightful comparison of BPPV and MD. By incorporating additional details on quality-of-life impacts and using diagnostic tools like HINTS, you can further enhance your analysis.

References

Johns, P., & Quinn, J. (2020). Clinical diagnosis of benign paroxysmal positional vertigo and vestibular neuritis. Canadian Medical Association Journal, 192(8), E182–E186. https://doi.org/10.1503/cmaj.190334

Li, W., Sun, J., Zhao, Z., Xu, J., Wang, H., Ding, R., & Zhang, Y. (2023). Efficacy of Epley’s manoeuvre plus betahistine in the management of PC-BPPV: A systematic review and meta-analysis. Medicine, 102(13), e33421–e33421. https://doi.org/10.1097/md.0000000000033421

Pauwels, S., Casters, L., Lemkens, N., Lemmens, W., Meijer, K., Meyns, P., van de Berg, R., & Spildooren, J. (2023). Gait and Falls in Benign Paroxysmal Positional Vertigo: A Systematic Review and Meta-analysis. Journal of Neurologic Physical Therapy: JNPT, 47(3), 127–138. https://doi.org/10.1097/NPT.0000000000000438

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In this discussion, we will compare two similar diagnoses, such as benign paroxysmal positional vertigo (BPPV) and Meniere’s disease (MD). The following will be reviewed, mutually each condition’s presentation, demographics, onset of symptoms, history of present illness, and associated risk factors. Additionally, commonalities and differences in pathophysiology, assessment techniques demonstrated during the physical assessment, appropriate diagnostic testing, diagnosing with further differential diagnoses to consider, and positive findings for each diagnosis. Lastly, this discussion will examine the management of both disorders, including any pharmacologic and nonpharmacologic treatments, client education, referral, and follow-up care.

Presentation

BPPV is one of the most common clinical forms of vestibular vertigo, affecting approximately 17-42% of patients. Patients with BPPV experience transitory, sudden episodes of vertigo during a change in head position. The lifetime prevalence of BPPV is estimated to be 2.4%, and the 1-year prevalence of BPPV in the elderly is significantly higher than in other age groups (Chen et al., 2020). It is seldom encountered in children and populations under age 35 years, where it is often related to head injuries. Patients with BPPV have recurring episodes of vertigo that last less than 60 seconds to minutes and are caused by variations in head motions relative to gravity. These vertigo spells may be accompanied by nausea and vomiting, a few complaints of “foggy or cloudiness” in sensorium, with no reports of hearing loss or other neurological symptoms. To validate BPPV, nystagmus must be observed while performing a stimulating maneuver. Several risk factors for BPPV include female gender, vitamin D deficiency, osteoporosis, migraines, head trauma, and high total cholesterol (TC) levels.

MD is a clinical syndrome that involves approximately 50 to 200 individuals per 100,000, with the highest prevalence occurring between the ages of 40 and 60 (Basura et al., 2020). MD symptoms typically manifest as “episodes” or “attacks.” In comparison to BPPV, which is the most prevalent cause of peripheral vertigo, MD episodes last longer and are also not reproducible by specific head movements (Wu et al., 2019). Characteristics of MD attacks include recurring feelings of rotational movement in their environment, also considered true vertigo. A crucial initial step in the approach to MD is to determine whether the patient’s sensation is true vertigo or another type of dizziness. Patients experience vertigo spells that may last 20 minutes to 12 hours (the majority last 2 to 3 hours; rarely, the attacks last up to 24 hours), as well as unilateral hearing loss and tinnitus, with or without auditory fullness or pressure, and hyperacusis (sensitivity to loud sounds) to the affected ear (Wu et al., 2019). Nausea, vomiting, sweating, and even diarrhea occur during these attacks, which are generally preceded by a sudden increase in unilateral nonpulsatile tinnitus. MD symptoms may fluctuate after their first presentation, with occurrences ranging in frequency and severity. According to some authors, excessive caffeine, or sodium intake, as well as fluctuations in barometric pressure, can cause vertigo. Furthermore, hearing loss usually becomes permanent as MD develops. Patients with bilateral MD may experience symptom variations in either ear and have a significantly diminished quality of life due to bilaterally impaired vestibular function and hearing. A familial history of MD, prior autoimmune disorders, allergies, head, or ear trauma, and, in rare cases, syphilis are risk factors.

Pathophysiology

BPPV is defined as a transitory, position-induced torsional, vertical, or horizontal nystagmus accompanied by vertigo. Symptoms are activated during certain positions of the head. The nystagmus’s brief latency, limited duration, fatigability, and reversibility upon returning to an erect position all contribute to the diagnosis. Any inner ear disorder that separates the otoconia tends to be capable of generating BPPV (Yetiser, 2019). Most often, BPPV is linked to calcium debris in the semicircular canals (SCC), which are meant to sense accelerations of the angular head. The impression of vertigo is brought on by debris in the SCC, which causes abnormal endolymph movement in response to positional changes. Secondary BPPV is identified when a clear etiology has been established. However, the source of the disease is commonly unknown; in these cases, idiopathic BPPV is diagnosed.

In comparison, MD is distinguished by recurring attacks of spontaneous, typically rotating vertigo, sensorineural hearing loss, tinnitus, and a sensation of fullness or pressure in the affected ear (Zou et al., 2022). Endolymphatic hydrops (ELH)—increased fluid within the inner ear organ—is seen or suspected (Wu et al., 2019). Though not all patients with ELH have a history of MD. MD can be caused by a variety of reasons, including trauma, infection, ischemia, allergies, autoimmune, and genetics. This shows a complex cause of the disease, but it also indicates that the origin of MD remains unknown.

Assessment

The goal of the physical examination should be to rule out any other possible explanations of the patient’s symptoms, especially any that could be fatal (stroke, for example). The HINTS (head-impulse, nystagmus, test-of-skew) assessment can be used to distinguish between vertigo caused by peripheral and central sources (Wu et al., 2019). It is always important to monitor orthostatic vital signs to rule out dizziness caused by dehydration or cardiogenic instability, which is commonly misdiagnosed as vertigo. Gait, tandem gait, Romberg, cranial nerve, and cerebellar testing are done when nonvestibular reasons have been ruled out. During the otoscopic examination, visualization for any structural abnormalities in the middle and external ears can confirm other causes for the patient’s complaints. The results of an otoscopy examination are usually normal in people with MD. Initial assessments of hearing can be made with a combination of performing the Weber and Rinne tuning fork tests.

BPPV can be diagnosed through clinical evaluation and by performing a Gadolinium-enhanced MRI if the data suggests central nervous system (CNS) lesion. However, based on distinctive symptoms, nystagmus induced by the Dix-Hallpike maneuver (also known as the Barany technique), and the absence of other abnormalities discovered during neurologic evaluation are sufficient to diagnose and require no additional examination. The Dix-Hallpike test involves promptly transferring the patient from a sitting to a supine position, with the head tilted 45° to one side. After around 20-30 seconds, the patient is restored to a seated position and the technique is repeated on the opposite side noting any nystagmus and vertiginous symptoms during positional changes.

For MD, patients must undergo bloodwork to rule out other conditions, diagnostic audiometric testing, and imaging. Audiometry often reveals low or combination low- and high-frequency sensorineural hearing loss (SNHL), along with normal mid-frequency hearing. Vestibular testing using videonystagmography is also completed on patients alleged of having MD (Wu et al., 2019). Results demonstrate a diminished caloric response in the afflicted ear. This testing can be arranged by a consultation to an otolaryngology-head and neck surgery (OHNS) service or by an otolaryngologist. An MRI of the head should be ordered for symptoms of unilateral tinnitus, SNHL, or both, and if intracranial disorders presented similarly as MD are suspected. Definitive criteria for MD include two or more spontaneous episodes of vertigo lasting 20 minutes to 12 hours, documented sensorineural hearing loss more than 30 decibels below and above 2 kHz, fluctuating hearing, tinnitus, and fullness in the affected ear, and exclusion of causes through other tests (Wu et al., 2019).

Diagnosis

Respective differential diagnoses for BPPV include otologic disorders such as Meniere’s disease, vestibular neuritis or labyrinthitis, vestibular paroxysmia, and superior canal dehiscence syndrome. Vestibular neuritis, also known as labyrinthitis, is characterized by a slow onset of vertigo that lasts for days to weeks, usually preceded by a viral prodrome. Vertigo can also be accompanied with persistent, severe degrees of nausea, vomiting, sweating, and pallor, can occur at rest, and does not always require postural adjustments to initiate. In vestibular paroxysmia, vascular compression of the vestibular nerve causes recurring, spontaneous episodes of vertigo lasting a few seconds to several minutes. There is no evidence of a crescendo-decrescendo pattern of nystagmus, and the positional triggers are different from BPPV. A favorable response to oxcarbazepine or carbamazepine medication serves as a diagnosis. Vertigo and oscillopsia, (the feeling that objects are swaying back and forth), are attacks of superior canal dehiscence syndrome that occur in response to loud noises, Valsalva maneuvers, or variations in the external auditory canal’s pressure. Unlike BPPV, vertigo in this syndrome is caused by pressure changes rather than positional changes in relation to gravity (BPPV for Ophthalmologists – EyeWiki, n.d.).

Differential diagnoses in relation to neurological disorders similar to BPPV may include vestibular migraine, central positional vertigo and other diagnoses of postural/orthostatic hypotension and persistent postural-perceptual dizziness (PPPD). In contrast to BPPV, vestibular migraine episodes have a shorter interval however are more persistent. Moreover, a migraine headache occurs concurrently with or after the vertigo spell. Cerebellar lesions may result in central positional vertigo. In distinction to BPPV, which experiences a fleeting nystagmus, the downbeat nystagmus is constant and lasts for the duration of the provoking position. Central positional nystagmus differs from anterior canal BPPV nystagmus in that it lacks a torsional component. In postural/orthostatic hypotension, transient vertigo or lightheadedness is present, but it only manifests as symptoms upon rising from a lying to seated position, not from shifting one’s head position in relation to gravity. Blood pressure readings taken when the patient is supine to standing can be used to make a diagnosis. Finally, persistent postural-perceptual dizziness (PPPD) is defined as having one or more dizziness, unsteadiness, or non-spinning vertigo symptoms for hours at a time, most of the time, for at least three months. The strength of these symptoms typically waxes and wanes. One symptom of PPPD is visual hypersensitivity when staring at complicated or moving objects (traffic, for example). BPPV and PPPD may cause or coexist, but BPPV is characterized by discrete episodes of vestibular symptoms and nystagmus linked to positional changes, but PPPD is not linked to head motion-induced vertigo and has persistent dizziness, unsteadiness, and non-spinning vertigo. Another name for this is visual variant vertigo (BPPV for Ophthalmologists – EyeWiki, n.d.).

For MD, differential diagnoses include BPPV, stroke or ischemia, vestibular migraine, vestibular schannoma, labyrinthitis, and vestibular neuritis. Clinical manifestations of stroke or ischemia exhibit vertigo that may occur within minutes, followed by nausea, vomiting, unbalance, dizziness, visual blurring, and drop attacks. Unlike MD, stroke symptoms are frequently persistent, non-fluctuating, and differ with indications of dysphagia, dysphonia, or other neurologic symptoms (Millennie, 2021). Hearing loss and tinnitus are typically not present in ischemic strokes. Vestibular schannoma symptoms include tinnitus, asymmetric hearing loss, persistent imbalance, and vertigo. In distinction to MD, vestibular schannoma is more likely to be a chronic imbalance than a severe episode of vertigo and hearing loss is unchanged. Ultimately, the other differential diagnoses for MD are interchangeable to many of the disorders mentioned regarding BPPV.

Management

BPPV may last for months or years, although it normally goes away spontaneously after a few weeks or months. For example, medications given to treat MD, are generally not advised since short episodes can repeat over an extended period and medication side effects frequently make dysequilibrium worse. One therapy strategy for BPPV is to have the patient engage in provocative maneuvers in a safe setting early in the day. This is because BPPV can be fatigue inducing. For the remainder of the day, symptoms are less noticeable. The goal of canalith repositioning procedure (CRP), which include the Epley maneuver, the Semont maneuver, and the Brandt-Daroff exercises, is to bring the errant canalith back to the utricle by moving the head through a sequence of precise positions. At home, the patient should attempt to prevent neck flexion or extension for one to two days following the completion of the Epley or Semont technique. They can repeat these movements as needed. The Brandt-Daroff exercises are performed three times a day, for a duration of approximately two weeks, or until the exercises no longer cause vertigo (Ear, Nose, and Throat Disorders – Merck Manuals Professional Edition, 2019). Patients can be referred to an ear, nose, throat (ENT) specialist, neurologist, or a vestibular physical therapist and follow-up care is not necessarily needed unless the CRP worsens vertigo or was unsuccessful.

MD has no known cure, although certain pharmacological and nonpharmacological therapies can help lessen the intensity and duration of vertigo episodes. When treating an acute attack, the goal is to relieve symptoms, subsequently ablative operations are options if the initial treatments are ineffective. Management of MD include medications like antiemetics, antihistamines, benzodiazepines, and diuretics. Stress-reduction counseling, education, as well as dietary and lifestyle adjustments to reduce alcohol and caffeine consumption are advised. Limiting sodium (<1.5 g/day) and monosodium glutamate has been linked to a decrease in episodes of vertigo by physiologically lowering pressure within the hydropic ear (Wu et al., 2019). Patients who experience severe debilitating episodes frequently and who do not respond to less invasive techniques are candidates for adjunctive surgery. About 95% of patients experience vertigo relief following an intracranial operation called vestibular neurectomy, which typically preserves hearing. Only in cases of severe previous hearing loss is a surgical labyrinthectomy performed (Ear, Nose, and Throat Disorders – Merck Manuals Professional Edition, 2019). More importantly, clients should be educated on sitting, lying down when dizziness spell occurs, resting during and after attacks, and utilizing preventative injuries or fall techniques. Patients with MD can be referred to otolaryngology–head and neck surgery, neurologist, vestibular rehabilitation therapist for balance recovery, or an audiologist to be fitted for hearing aids in progressive MD.

References

Basura, G. J., Adams, M. E., Monfared, A., Schwartz, S. R., Antonelli, P. J., Burkard, R., Bush, M. L., Bykowski, J., Colandrea, M., Derebery, J., Kelly, E. A., Kerber, K. A., Koopman, C. F., Kuch, A. A., Marcolini, E., McKinnon, B. J., Ruckenstein, M. J., Valenzuela, C. V., Vosooney, A., & Walsh, S. A. (2020). Clinical Practice Guideline: Ménière’s Disease Executive Summary. Otolaryngology–Head and Neck Surgery, 162(4), 415–434. https://doi.org/10.1177/0194599820909439

Benign Paroxysmal Positional Vertigo (BPPV) for ophthalmologists – EyeWiki. (n.d.). Eyewiki.aao.org. Retrieved July 9, 2024, from https://eyewiki.aao.org/Benign_Paroxysmal_Positional_Vertigo_(BPPV)_for_ophthalmologists#cite_note-:5-8

Chen, J., Zhao, W., Yue, X., & Zhang, P. (2020). Risk Factors for the Occurrence of Benign Paroxysmal Positional Vertigo: A Systematic Review and Meta-Analysis. Frontiers in Neurology, 11. https://doi.org/10.3389/fneur.2020.00506

Ear, Nose, and Throat Disorders – Merck Manuals Professional Edition. (2019). Ear, Nose, and Throat Disorders – Merck Manuals Professional Edition. Merck Manuals Professional Edition. https://www.merckmanuals.com/professional/ear

Millennie, Helena & Munir, Badrul & Afif, Zamroni & Damayanti, Ria & Nandar, Shahdevi. (2021). MENIERE’S DISEASE. JPHV (Journal of Pain, Vertigo and Headache). 2. 18-21. 10.21776/ub.jphv.2021.002.01.5.

Wu, V., Sykes, E. A., Beyea, M. M., Simpson, M. T. W., & Beyea, J. A. (2019). Approach to Ménière disease management. Canadian Family Physician, 65(7), 463–467. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738466/

Yetiser, S. (2019). Review of the pathology underlying benign paroxysmal positional vertigo. Journal of International Medical Research, 48(4), 030006051989237. https://doi.org/10.1177/0300060519892370

‌ Zou, W., Li, Q., Peng, F., & Huang, D. (2022). Worldwide Meniere’s disease research: A bibliometric analysis of the published literature between 2002 and 2021. Frontiers in Neurology, 13, 1030006. https://doi.org/10.3389/fneur.2022.1030006

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