Cause Of Benign Paroxysmal Positional Vertigo Research Articles

5155 Benign Paroxysmal Positional Vertigo as a Potential Manifestation of Hypothyroidism, a Case Report

Abstract Disclosure: M. Ahmad: None. M. Herrera: None. D. Deyar: None. P. Gill: None. Introduction: Benign Paroxysmal Positional Vertigo (BPPV) is a vestibular disorder characterized by recurrent episodes of vertigo triggered by specific head movements. The pathophysiology of BPPV involves the displacement of otoconia within the semicircular canals of the inner ear. However, emerging evidence suggests that BPPV may manifest as a consequence of hypothyroidism. In this case report, we present a clinical case of a patient who exhibited symptoms of BPPV and was subsequently diagnosed with hypothyroidism. We aim to elucidate the relationship between these two seemingly distinct conditions and highlight the importance of considering hypothyroidism as a potential cause of BPPV. Case presentation: A 56-year-old female with a past medical history of migraines presented to the hospital for three days of dizziness. She had multiple bouts of vomiting and right-sided headaches similar to her prior migraine headaches. The patient also noted dry skin, constipation, and hair loss for the past few months. The patient’s vital signs were as follows: temperature: 35.6 C, heart rate: 65 beats per minute, blood pressure: 153/66 mmHg, and respiratory rate: 18 breaths per minute. On physical examination, the Dix-Hallpike maneuver was positive on the right side and the patient was noted to have diffusely dry skin. The patient’s labs were significant for the following: sodium: 137 mmol/L, potassium: 3.7 mmol/L, creatinine: 0.88 mg/dL, thyroid stimulating hormone: 31.2 uIU/ml, free T4 ng/dL, hemoglobin: 10.8 g/dL (MCV of 87), and TPO antibody: 2350 IU/ml. The patient underwent CT and MRI imaging of the brain without contrast, which was negative for any acute intracranial abnormalities. The patient was diagnosed with BPPV and hypothyroidism secondary to Hashimoto’s thyroiditis and subsequently underwent vestibular physical therapy with improvement in her vertigo and was started on 112 mcg of levothyroxine daily. She is set to follow up with her primary care provider as an outpatient. Discussion: BPPV generates significant repercussions to an individual’s quality of life, autonomy, and functionality. Hypothyroidism is a common condition characterized by thyroid hormone deficiency that has been linked with a wide array of clinical manifestations, including vestibular disturbances. Autoimmune dysfunction, anomalies of the endolymphatic flow and low perfusion to the inner ear are potential etiological factors that can explain the relationship between thyroid disorders with BPPV. Some studies mention that thyroid autoantibodies could induce autoimmune-complex deposition in the inner ear, which might change the endolymphatic flow and induce BPPV. Raising awareness regarding this potential manifestation of hypothyroidism can guide clinical and diagnostic decisions that improve patient care, especially in individuals under evaluation for BPPV with other symptoms of hypothyroidism. Presentation: 6/3/2024

Residual dizziness after BPPV management: exploring pathophysiology and treatment beyond canalith repositioning maneuvers.

Despite the high success rate of canalith repositioning maneuvers (CRMs) in the treatment of benign paroxysmal positional vertigo (BPPV), a growing number of patients report residual dizziness symptoms that may last for a significant time. Although the majority of BPPV cases can be explained by canalolithiasis, the etiology is complex. Consideration of the individual patient's history and underlying pathophysiology of BPPV may offer the potential for treatment approaches supplementary to CRMs, as well as a promising alternative for patients in whom CRMs are contraindicated. This article provides a summary of the possible underlying causes of BPPV and residual dizziness, along with suggestions for potential management options that may be considered to relieve the burden of residual symptoms.

Revisiting pathophysiology of benign paroxysmal positional vertigo: a review

Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. There are several possible underlying causes of BPPV, although the idiopathic form is the most common. BPPV is characterized by brief recurrent episodes of vertigo that are triggered by changes in head position. Although BPPV is a benign vestibular disorder, it can be a severe and disabling problem for some of patients. The pathophysiology of BPPV is still unclear. The pathophysiology for BPPV is complex and the underlying mechanism is related to free-floating debris/otoliths in the semicircular canal (canalolithiasis) or debris/otoliths attached to the cupula (cupulolithiasis). These otolith/debris are originally accumulated after detachment from the neuroepithelium of the utricular macula secondary to degeneration. BPPV can occur following other vestibular disorders. In the majority of cases, the triggering factors are unknown. Some patients of BPPV have a history of previous inner ear diseases such as Meniere’s disease or acute unilateral peripheral vestibulopathy. This clinical entity is well-defined in medical literature and usually effectively treated by certain physical maneuvers. However, the pathophysiology is still obscure and is being critically discussed in this article, which reviews the details pathological mechanism for BPPV. This review article will discuss that aging, trauma, migraine, Meniere’s disease, vestibular neuronitis, and vitamin-D deficiency are the most commonly investigated etiopathological factors resulting in BPPV.

Comparing Therapeutic Maneuvers in Posterior Canal Benign Paroxysmal Positional Vertigo

Context: Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo accounting for around 24% of all peripheral vestibular abnormalities and the posterior semicircular canal being the most affected. The most common cause of BPPV is idiopathic, others being inner ear disorders, trauma, infection, and increasing age. Objective: This study evaluated the efficacy of Epley’s maneuver alone and Epley’s maneuver with Brandt–Daroff exercises in the management of posterior semicircular canal BPPV, thereby comparing the recurrence rate after treatment in both groups. Materials and Methods: The study was a randomized prospective clinical trial with parallel and superiority trial design where 94 consecutive patients with posterior semicircular canal BPPV and fulfilling the inclusion criteria were enrolled into two Groups A = 47 and B = 47. All subjects underwent detailed history, examination, and assessment with UCLA dizziness questionnaire and videonystagmography. Group A patients received Epley’s maneuver while group B received Epley’s maneuver with Brandt–Daroff exercises as the treatment, with follow-up done on the 1st and 2nd weeks and after 1 month. Results: The age group of the majority of the patients in the study ranged between 51 and 60 years. The percentage of females in the study was 54.3% and males 45.7%. Results showed significant improvement in vertigo and nystagmus in both groups, with Group B having lesser recurrence during the follow-up visits. Conclusion: Both Epley’s maneuver and Brandt–Daroff exercises are ideal means of treatment, but a combined approach of the two maneuvers yields better outcome in terms of symptomatic resolution and less recurrence.

Benign paroxysmal positional vertigo in pediatric age group: a review

Vertigo is not common in the pediatric age group, but probably more often than was formerly thought. Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. It consists of the short duration of vertigo attacks found in a definite head position. The exact cause of BPPV is related to the idiopathic detachment of otoconia from the utricular membrane. The prevalence of BPPV in children is lower than in the adult age group. In children with BPPV, the symptoms consist of transitory rotational vertigo and torsional/ vertical/ horizontal or mixed nystagmus, depending on the position of the intra-labyrinthine otoliths, with latency and intensity in a typical crescendo-decrescendo pattern and it is exhaustible, reversible and fatiguing similar to adults. The diagnosis of BPPV can be accurately done by taking a detailed medical history, audiogram, and by use of positional testing. In children, BPPV can be successfully diagnosed and treated. In most cases, pediatric patients could not express details of their symptoms, and clinicians cannot always obtain adequate medical histories and determine their objective signs. So, it is not easy to study the BPPV in children. There are only a few articles describing BPPV in the pediatric age group, and therefore this subject is not well known to most otolaryngologists and clinicians. This review article discusses the epidemiology, etiopathology, clinical manifestations, diagnosis, and treatment of BPPB in the pediatric age group.

Study on Platelet Indices in Benign Paroxysmal Positional Vertigo

Objectives: Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of dizziness. Even though the etiology of BPPV has been widely studied, the exact mechanism remains still unclear. One of the possible factors explaining the pathophysiology of BPPV is ischemia of vestibule. In the present study, we have focused on the platelet indices including mean platelet volume (MPV), platelet distribution width (PDW), and platelet crit (PCT) to assess a risk of vestibule ischemia causing BPPV.Methods: From January 2021 to March 2021, a retrospective review was performed on 39 patients diagnosed with BPPV through vestibular nystagmography. For each platelet indices, a comparative analysis was conducted between the patient group and control group.Results: There were no significant differences when the platelet, MPV, PDW, and PCT values were compared between the study and control group. Rather, the control group showed higher PDW value than the study group.Conclusions: Ischemia of vestibule is one of the well-known causes of BPPV, but the current study showed that BPPV cannot be explained by the vestibule ischemia itself. Further studies are needed to identify the potential of ischemia regarding BPPV by approaching with other methods with a large study group.

Objective diagnostic possibility in the differentiation of idiopathic and secondary benign paroxysmal positional vertigo

Introduction: Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder. The most important symptom is vertigo, which is triggered by changes in head position and sometimes is accompanied by vegetative symptoms. Furthermore, etiology may be subcategorized into idiopathic and secondary (connected to other vestibular disorder, like Ménière's disease, vestibular neuritis, or vestibular migraine). Aim: To identify such parameter of ultrasound-computer-craniocorpography (US-COMP-CCG), which could be useful in the differentiation of idiopathic and secondary BPPV. Material and method: 135 patients suffering from BPPV and 140 normal vestibular functioning patients were examined with UC-COMP-CCG. Statistical analysis was completed by using IBM SPSS V24 software. Results: 109 patients suffered from idiopathic BPPV (i-BPPV), and 26 patients from secondary BPPV (s-BPPV). Parameters indicating the imbalance were observed in both the standing test and the stepping test. Respectively, remarkable results were given in the forehead covering and the self-spin parameter. Conclusion: By applying and examining both study groups with US-COMP-CCG, we were able to use modern diagnostics and thus have an objective evaluation based on their properties. The objective results from the US-COMP-CCG parameters show the deterioration of the vestibular system as well as the change in values, based on the cause of BPPV in secondary cases. Orv Hetil. 2020; 161(6): 208-213.

Review of the pathology underlying benign paroxysmal positional vertigo.

The pathophysiological mechanism underlying benign paroxysmal positional vertigo (BPPV) is related to free-floating debris/otoliths in the semicircular canal (canalolithiasis) or debris/otoliths attached to the cupula (cupulolithiasis). These debris/otoliths are considered to originally accumulate after detachment from the neuroepithelium of the utricular macula secondary to a type of degeneration. An idiopathic form, which is assumed to occur spontaneously, is diagnosed when the causative pathology is obscure. However, an association between various other systemic or inner ear conditions and BPPV has been reported, indicating the existence of secondary BPPV. This study was performed to present the first review of the pathology underlying BPPV following a complete PubMed/Medline search. In total, 1932 articles published from 1975 to 2018 were reviewed. The articles were classified according to 17 potentially causative factors (aging; migraine; Meniere’s disease; infection; trauma; idiopathic sudden sensorineural hearing loss; sleeping habits; osteoporosis and vitamin D insufficiency; hyperglycemia and diabetes mellitus; chronic head and neck pain; vestibule or semicircular canal pathology; pigmentation disorders; estrogen deficiency; neurological disorders; autoimmune, inflammatory, or rheumatologic disorders; familial or genetic predisposition; and allergy). A discussion of the underlying cause of BPPV for each factor is presented.

Evaluation of benign paroxysmal positional vertigo following Le Fort I osteotomy

The Le Fort I osteotomy is widely used to correct dentofacial deformities. Benign paroxysmal positional vertigo (BPPV) is a common vestibular end organ disorder characterized by short, often recurrent episodes of vertigo. Head trauma is one of the known causes of BPPV. During pterygoid osteotomy, the surgical trauma induced by percussion with the surgical mallet and osteotomes can displace otoliths into the semicircular canal, resulting in BPPV. The aim of this study was to evaluate the potential risk of occurrence of BPPV in individuals undergoing Le Fort I osteotomy. Twenty-three patients were included in this study. The Dix–Hallpike manoeuvre, positional tests using electronystagmography, and vestibular evoked myogenic potential (VEMP) tests were performed 1 week before surgery (T0), 1 week after surgery (T1), and 1 month after surgery (T2). The results were compared statistically. BPPV was observed in three patients. Eleven patients had nystagmus at the T1 evaluation and seven at the T2 evaluation. The difference between the T0 and T1 time points was statistically significant (P=0.001). BPPV is a possible complication of Le Fort I osteotomy. Surgeons should be aware of this complication, and the diagnosis of BPPV should be considered in patients who have undergone Le Fort I osteotomy.

Pain and other symptoms in patients with chronic benign paroxysmal positional vertigo (BPPV)

Background and aimA diagnosis of chronic benign paroxysmal positional vertigo (BPPV) is based on brief attacks of rotatory vertigo and concomitant nystagmus elicited by rapid changes in head position relative to gravity. However, the clinical course of BPPV may vary considerably from a self-limiting to a persisting and/or recurrent disabling problem. The authors’ experience is that the most common complaints of patients with chronic BPPV are nautical vertigo or dizziness with other symptoms including neck pain, headache, widespread musculoskeletal pain, fatigue, and visual disturbances. Trauma is believed to be the major cause of BPPV in individuals younger than fifty years. Chronic BPPV is associated with high morbidity. Since these patients often suffer from pain and do not have rotatory vertigo, their symptoms are often attributed to other conditions. The aim of this study was to investigate possible associations between these symptoms and chronic BPPV. MethodsDuring 2010 a consecutive prospective cohort observational study was performed. Diagnostic criteria: (A) BPPV diagnosis confirmed by the following: (1) a specific history of vertigo/dizziness evoked by acceleration/deceleration, (2) nystagmus in the first position of otolith repositioning maneuvers, and (3) appearing and disappearing nystagmus during the repositioning maneuvers; (B) the disorder has persisted for at least six months. (C) Normal MRI of the cerebrum. Exclusion criteria: (A) Any disorder of the central nervous system (CNS), (B) migraine, (C) active Ménière's disease, and (D) severe eye disorders. Symptom questionnaire (‘yes or no’ answers during a personal interview) and Dizziness Handicap Inventory (DHI) were used. ResultsWe included 69 patients (20 males and 49 females) with a median age of 45 years (range 21–68 years). The median duration of the disease was five years and three months. The video-oculography confirmed BPPV in more than one semicircular canal in all patients. In 15% there was a latency of more than 1min before nystagmus occurred. The Dizziness Handicap Inventory (DHI) median score was 55.5 (score >60 indicates a risk of fall). Seventy-five percent were on 50–100% sick leave. Eighty-one percent had a history of head or neck trauma. Nineteen percent could not recall any history of trauma. In our cohort, nautical vertigo and dizziness (81%) was far more common than rotatory vertigo (20%). The majority of patients (87%) reported pain as a major symptom: neck pain (87%), headache (75%) and widespread pain (40%). Fatigue (85%), visual disturbances (84%), and decreased concentration ability (81%) were the most frequently reported symptoms. In addition, unexpected findings such as involuntary movements of the extremities, face, neck or torso were found during otolith repositioning maneuvers (12%). We describe one case, as an example, how treatment of his BPPV also resolved his chronic, severe pain condition. ConclusionThis observational study demonstrates a likely connection between chronic BPPV and the following symptoms: nautical vertigo/dizziness, neck pain, headache, widespread pain, fatigue, visual disturbances, cognitive dysfunctions, nausea, and tinnitus. ImplicationsPatients with complex pain conditions associated with nautical vertigo and dizziness should be evaluated with the Dizziness Handicap Inventory (DHI)-questionnaire which can identify treatable balance disorders in patients with chronic musculoskeletal pain.

Post-traumatic camel-related benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is a common form of dizziness. The causes of BPPV are not yet known but a relationship between the onset of vertigo and head trauma has been found. Among the causes of head injury related to BPPV, dropping off a camel has not been reported in literature yet. We describe two cases of persons that fell off a camel during a safari in Middle East countries. After the fall they reported vertigo symptoms that were not interpreted as BPPV. When they returned to Italy, due to symptoms persistence, they were referred to our ENT practice: we found evidence of BPPV. In a case it was a bilateral BPPV (bBPPV). Falling off a camel may be a relevant cause of BPPV. We suggest a correct evaluation of the labyrinth for BPPV with the appropriate diagnostic maneuvers and, if necessary, a treatment with repositioning maneuvers.

良性発作性頭位めまい症の回旋性眼振の垂直成分

Benign paroxysmal positional vertigo (BPPV), one of the most common diseases of peripheral vestibular origin, is characterized by transient vertigo accompanied by benign paroxysmal positional nystagmus (BPPN) provoked by turning over in bed, lying down or sitting up. BPPN with a torsional component, short latency and a crescendo-decrescendo mode, is provoked by positional testing and disappears within 30 sec. The direction of the torsional nystagmus, provoked by lying down, reverses by sitting up. The nystagmus may decrease by repeated provocations as an adaptation. Canalolithiasis of the posterior canal is widely accepted as a cause of BPPV, because BPPN is well predicted and BPPV is successfully treated by Epley's canalith repositioning procedure on the basis of this hypothesis. Canalolithiasis of both the horizontal and anterior canals has also been reported as BPPV-variants. In this study, BPPN recorded by an infrared CCD camera and video recorder, and the incidence and meaning of the vertical component of BPPN were investigated in 110 cases of BPPV with torsional BPPN. Out of all 110 cases, up beating vertical component appeared in 39 (35.5%), down beating in 24 (21.8%) and no vertical component in 47 cases (42.7%), when torsional BPPN was provoked by lying down. Horizontal nystagmus of the direction changing type was also observed in 4 cases. According to the canalolithiasis hypothesis, upward and downward vertical components triggered by lying down should occur in the posterior and anterior canal types, respectively. Pure torsional positional nystagmus provoked by positioning was assumed to occur in the crus communis type, in which free-floating endolymph particles remain in the crus communis of the labyrinth.

良性発作性頭位めまい症と睡眠頭位

This study indicates that head position during sleep is likely to contribute to the pathogenesis of benign paroxysmal positional vertigo (BPPV). Seventy-two patients, consisting of 54 with posterior semicircular canal BPPV and 18 with lateral semicircular canal BPPV, were examined (BPPV group). Seventy-six healthy individuals of statistically the same age and sex as those of the BPPV group were also examined (healthy group).This study revealed that the percentage of people who always sleep in the same head position, particularly with the right side or left side down, amounted to 61 % of the BPPV group and 24% of the healthy group, which was significantly different (p<0.005). In 39 BPPV patients, (mean follow-up of 7.7 years) the recurrence rate was 41%, and the persistence rate was 13%. When patients were consulted to avoid having a fixed head position during sleep, the recurrence rate decreased to 18%, and the persistence rate decreased to 3%. In addition, almost all recurrent patients were ones who could not avoid a fixed head position during sleep. There was no correlation between the affected side of BPPV and the particular head position during sleep. In patients with latent inner ear disorders and/or utricular damage of unknown origin, habitually sleeping with the head position down on the right side or left side might induce otoconial detachment, causing BPPV and recurrence or persistence of BPPV. As an important possible cause of BPPV, the head position during sleep should be taken into consideration.

頭位めまい症に対する浮遊耳石置換法の効果

To investigate the pathophysiology of benign paroxysmal positional vertigo (BPPV), we observed positional nystagmus and assessed the efficacy of the canalith repositioning procedure (CRP). Nystagmus was recorded using an infrared CCD camera. Subjects were 36 patients who exhibited typical rotatory nystagmus of BPPV with Hallpike maneuvers. The therapy given to the control group (Group A, n=18) was medication only, while Group B (n=18) was treated by both CRP and medication. In almost all patients, rotatory nystagmus was provoked by slow position change from the healthy ear down (head hanging position with a 45-degree tilt to the healthy side) to the affected ear down (head hanging position with a 45-degree tilt to the affected side). This phenomenon indicates that rapid movement is not necessary for provocation, and a 45-degree off sagittal tilt indicates that the lesion is in the posterior semicircular canal. The period of disease in Group B was significantly shorter than that in Group A. In Group B, CRP was effective in 16 patients (89%). We conclude that free-moving particles in the posterior semicircular canal is the cause of BPPV. We suggest that rotatory positional nystagmus is a result of ampullofugal flow of sinking particles in the posterior semicircular canal and secondary ampullof ugal flow in the anterior semicircular canal.

Benign paroxysmal positional vertigo as a complication of postoperative bedrest.

Seven cases of benign paroxysmal positional vertigo (BPPV) after operation were reported, occurring between the fourth and 14th postoperative day. In three of the seven cases, the condition occurred when the patients first arose from bed after 5 to 6 days of postoperative bedrest. In two cases, BPPV occurred when patients moved their head while maintaining strict bedrest. In the other two cases, it occurred 1 to 4 days after patients had been released from bedrest. The cause of BPPV was considered to be postoperative bedrest which might have facilitated the deposition of precipitate on the cupula of the posterior semicircular canal. The prognosis was good, and all the patients recovered within 20 days.