Łagodne napadowe położeniowe zawroty głowy
Patofizjologia i mechanizm

Łagodne napadowe położeniowe zawroty głowy (BPPV) są najczęstszą przyczyną zawrotów głowy o etiologii obwodowej, wynikającą z przemieszczenia kryształów węglanu wapnia (otokonia) z łagiewki do kanałów półkolistych ucha wewnętrznego, najczęściej do kanału półkolistego tylnego (80-90% przypadków). Patomechanizm BPPV opiera się na dwóch mechanizmach: kanalitoliazie, gdzie luźne otokonia swobodnie przemieszczają się w endolimfie kanału, wywołując krótkotrwałe (<1 min) epizody zawrotów głowy i oczopląsu z opóźnieniem po zmianie pozycji głowy, oraz kupulolitiazie, gdzie otokonia przylegają do kopuły bańkowatej, powodując dłużej utrzymujące się objawy. BPPV może mieć charakter idiopatyczny (50-70% przypadków), związany z wiekową degeneracją narządu przedsionkowego, lub wtórny, powiązany z urazem głowy, chorobami ucha wewnętrznego, migreną, niedokrwieniem, leczeniem ototoksycznym czy zaburzeniami metabolicznymi (np. osteoporozą, niedoborem witaminy D).

Patogeneza łagodnych napadowych położeniowych zawrotów głowy (BPPV)

Łagodne napadowe położeniowe zawroty głowy (BPPV) stanowią najczęstszą przyczynę zawrotów głowy pochodzenia obwodowego. Zaburzenie to charakteryzuje się krótkimi, nawracającymi epizodami zawrotów głowy wywołanymi określonymi zmianami pozycji głowy w stosunku do siły grawitacji. Aby zrozumieć mechanizm powstawania BPPV, należy najpierw poznać anatomię i fizjologię narządu przedsionkowego odpowiedzialnego za utrzymanie równowagi.12

Anatomia i fizjologia narządu przedsionkowego

Narząd przedsionkowy (błędnik) w uchu wewnętrznym składa się z trzech kanałów półkolistych wypełnionych płynem (endolimfą), które zawierają delikatne czujniki włoskowate monitorujące ruchy głowy. Inne istotne struktury ucha wewnętrznego to narządy otolitoweworeczek (saccule) i łagiewka (utricle), które zawierają kryształy węglanu wapnia (otokonia), reagujące na siłę grawitacji.12

W warunkach prawidłowych narządy otolitowe umożliwiają wykrywanie przyspieszeń liniowych i położenia głowy względem siły grawitacji, podczas gdy kanały półkoliste wykrywają przyspieszenia kątowe (obroty głowy). Kiedy głowa pozostaje w spoczynku, nie występuje stymulacja kanałów półkolistych. Natomiast podczas ruchu głowy przepływ endolimfy pobudza komórki rzęsate w wypustkach bańkowatych (ampułkach) kanałów, przekazując do mózgu informacje o zmianie położenia.12

Mechanizm powstawania BPPV

BPPV występuje, gdy kryształy węglanu wapnia (otokonia) odrywają się od łagiewki i przemieszczają do kanałów półkolistych ucha wewnętrznego, gdzie nie powinny się znajdować. Kanał półkolisty tylny jest najczęściej zajętym kanałem (80-90% przypadków), ponieważ jest on najbardziej zależny od grawitacji częścią błędnika.123

W BPPV istnieją dwa główne mechanizmy patofizjologiczne, które wyjaśniają powstawanie objawów: kanalitoliaza i kupulolitiaza.12

Kanalitoliaza

Kanalitoliaza (canalithiasis, dosłownie „kamienie w kanale”) występuje, gdy wolno przemieszczające się cząsteczki otokonialne znajdują się w części kanałowej kanałów półkolistych. Teoria ta została zaproponowana przez Epley’a w 1980 roku i jest obecnie uznawana za główny mechanizm powstawania klasycznego BPPV.12

W kanalitolizie luźne cząsteczki otokonialne przemieszczają się swobodnie w endolimfie kanału półkolistego pod wpływem grawitacji, gdy pozycja głowy zmienia się. Ten ruch cząsteczek powoduje opór hydrodynamiczny, który wywołuje przepływ endolimfy, prowadząc do przemieszczenia kopuły i stymulacji komórek rzęsatych. Efektem tego jest nieprawidłowa informacja o ruchu, która jest przesyłana do mózgu, wywołując zawroty głowy i oczopląs.12

Kanalitoliaza lepiej wyjaśnia charakterystyczne cechy BPPV, takie jak opóźnienie (latencja) wystąpienia objawów po zmianie pozycji, przemijający charakter oczopląsu oraz odwrócenie kierunku oczopląsu po powrocie do pozycji pionowej.12

Kupulolitiaza

Kupulolitiaza (cupulolithiasis, dosłownie „kamienie w kopule”) odnosi się do sytuacji, gdy cząsteczki otokonialne przylegają do kopuły grzebienia bańkowatego. Teoria ta została zaproponowana przez Harolda Schuknechta w 1962 roku jako „teoria ciężkiej kopuły”.12

W kupulolitiazie cząsteczki otokonialne nie są swobodnie przemieszczające się, lecz przylegają do kopuły, zwiększając jej ciężar. To powoduje, że kopuła staje się wrażliwa na siły grawitacyjne. W rezultacie przy zmianie pozycji głowy dochodzi do nieprawidłowego wychylenia kopuły, co prowadzi do patologicznego odczucia ruchu.12

W przeciwieństwie do kanalitoliazy, kupulolitiaza charakteryzuje się dłuższym utrzymywaniem się oczopląsu i zawrotów głowy, aż do momentu, gdy głowa zostanie przesunięta z pozycji wywołującej objawy lub gdy mózg zdecyduje się na stłumienie niepożądanej odpowiedzi.1

Różnice między kanalitoliazą a kupulolitiazą

Istotne różnice między tymi dwoma mechanizmami obejmują:

  • W kanalitolizie oczopląs i zawroty głowy zwykle trwają krócej niż minutę, ponieważ cząsteczki otokonialne przestają się przemieszczać po pewnym czasie w danej pozycji.1
  • W kupulolitiazie objawy utrzymują się dłużej, dopóki głowa nie zostanie przesunięta z pozycji wywołującej objawy.1
  • Kanalitoliaza lepiej wyjaśnia opóźnienie w wystąpieniu objawów po zmianie pozycji głowy oraz odwrócenie kierunku oczopląsu po powrocie do pozycji wyjściowej.12

Obecnie uważa się, że oba mechanizmy mogą współistnieć i odpowiadać za różne podtypy BPPV.12

Etiopatogeneza BPPV

BPPV można podzielić na dwie kategorie w zależności od przyczyny:

BPPV idiopatyczne (pierwotne)

Około 50-70% przypadków BPPV występuje bez znanej przyczyny i określa się je jako BPPV idiopatyczne lub pierwotne.1 W tych przypadkach uważa się, że przyczyną jest degeneracja narządu przedsionkowego związana z wiekiem, powodująca osłabienie połączeń włóknistych między otokoniami i ich oderwanie.12

Z wiekiem dochodzi do zmniejszenia ilości kryształów węglanu wapnia w otolitach. Ten proces demineralizacji osłabia połączenia włókniste między otokoniami, prowadząc do pęknięć lub fragmentacji, mniejszej stabilności otolitów i przemieszczenia otokoniów z łagiewki do kanałów półkolistych.1

BPPV wtórne

Pozostałe przypadki określa się jako BPPV wtórne i są one często związane z innymi chorobami lub czynnikami, takimi jak:12

  • Uraz głowy – najczęstsza przyczyna BPPV u osób poniżej 50. roku życia (8-20% przypadków BPPV przypisuje się urazom).12
  • Choroby ucha wewnętrznegozapalenie neuronu przedsionkowego, zapalenie błędnika, choroba Ménière’a.12
  • Migrena – istnieje silny związek między BPPV a migreną. Proponowane mechanizmy łączące te dwa stany to czynniki genetyczne i uszkodzenie naczyniowe błędnika.12
  • Niedokrwienie – niewystarczające ukrwienie układu przedsionkowo-podstawnego.1
  • Przyczyny jatrogenne – operacje ucha, długotrwałe unieruchomienie na plecach (np. podczas zabiegu stomatologicznego), leczenie lekami ototoksycznymi (np. gentamycyną).12
  • Zaburzenia metaboliczne – ostatnie badania wykazały związek między BPPV a osteoporozą oraz niedoborem witaminy D.12

W porównaniu z BPPV idiopatycznym, przypadki wtórne częściej dotyczą obu uszu (postać obustronna), wymagają więcej niż jednego leczenia i częściej nawracają.1

Czasowy przebieg BPPV

BPPV często opisuje się jako „samoograniczającą się” chorobę, ponieważ objawy często ustępują lub znikają w ciągu 1-2 miesięcy od wystąpienia.1 Uważa się, że luźne otokonia są aktywnie reabsorbowane przez „ciemne komórki” błędnika.1

Jednak BPPV często nawraca. Około 1/3 pacjentów doświadcza nawrotu w ciągu pierwszego roku po leczeniu, a w ciągu pięciu lat u około połowy pacjentów występuje nawrót.1 Czasowy przebieg BPPV charakteryzuje się spontanicznymi remisjami, które zwykle występują po kilku dniach do kilku tygodni, oraz nawrotami, które występują u około 50% pacjentów.1

Mechanizm powstawania objawów BPPV

Symptomatologia BPPV jest bezpośrednim wynikiem nieprawidłowych sygnałów z kanałów półkolistych, które tworzą złudzenie ruchu.1 Gdy cząsteczki otokonialne przemieszczają się w kanałach półkolistych, następuje nieprawidłowa stymulacja komórek rzęsatych, co prowadzi do przesyłania fałszywych informacji do mózgu o ruchu głowy, mimo że głowa jest nieruchoma.12

Fałszywe informacje nie pasują do tego, co odbiera drugie ucho, co widzą oczy lub co robią mięśnie i stawy. Ta niezgodność informacji jest przez mózg interpretowana jako zawroty głowy, które zwykle trwają krócej niż minutę.12

Z czasem mózg może reagować coraz słabiej na dezorientujące sygnały wywołane przez cząsteczki w uchu wewnętrznym. Proces ten nazywa się kompensacją i zachodzi najszybciej, jeśli pacjent wykonuje normalne ruchy głową, nawet jeśli ruchy te powodują uczucie wirowania.12

Anatomiczne predylekcje BPPV

Kanał półkolisty tylny jest najczęściej zajętym kanałem w BPPV (80-90% przypadków), ponieważ jest on najbardziej zależną od grawitacji częścią błędnika przedsionkowego.12 Jest to podobne do sytuacji, gdy zanieczyszczenia gromadzą się w zagięciu U-kształtnym pod zlewem.1

Rzadziej zajęte są kanał półkolisty boczny (poziomy) i kanał półkolisty górny (przedni). W rzadkich przypadkach BPPV może dotyczyć wielu kanałów jednocześnie.1

Interesujące jest, że BPPV w chorobie Ménière’a często dotyka kanału półkolistego poziomego, co może być związane z rozwojem otolitiazy w tej chorobie. Rozszerzenie błędnika błoniastego w chorobie Ménière’a może prowadzić do utraty jego elastyczności, oderwania otolitów i częściowej niedrożności.1

Podsumowanie patogenezy BPPV

Łagodne napadowe położeniowe zawroty głowy (BPPV) są wynikiem mechanicznego zaburzenia ucha wewnętrznego, polegającego na przemieszczeniu kryształów węglanu wapnia (otokoniów) z łagiewki do kanałów półkolistych. Przemieszczenie to może wystąpić spontanicznie (BPPV idiopatyczne) lub w wyniku urazu, choroby czy innych czynników (BPPV wtórne).12

Dwa główne mechanizmy patofizjologiczne BPPV to kanalitoliaza (wolno przemieszczające się cząsteczki w kanale) i kupulolitiaza (cząsteczki przylegające do kopuły). Oba mechanizmy prowadzą do nieprawidłowej stymulacji narządu przedsionkowego podczas zmiany pozycji głowy, co skutkuje zawrotami głowy i oczopląsem.12

Zrozumienie patofizjologii BPPV, zarówno kanalitoliazy, jak i kupulolitiazy, umożliwiło opracowanie różnych technik repozycjonowania, mających na celu przesunięcie przemieszczonych otokoniów z powrotem do łagiewki, gdzie są one łatwiej resorbowane i nie powodują objawów.12

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 12.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Benign Paroxysmal Positional Vertigo – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470308/
    Benign paroxysmal positional vertigo (BPPV) occurs due to the displacement of calcium-carbonate crystals or otoconia within the fluid-filled semicircular canals of the inner ear. […] Approximately 50% to 70% of BPPV cases occur with no known cause and are referred to as primary or idiopathic BPPV. […] The remaining cases are called secondary BPPV and are often associated with an underlying pathology, such as head trauma, vestibular neuronitis, labyrinthitis, Mnire disease, migraine, ischemia, and iatrogenic causes. […] With BPPV, otoconia (also known as „otoliths” or „canaliths”) dislodge and settle within the endolymph of the semicircular canals. […] When the head remains static, there is no stimulus. […] With motion, however, the displaced otoconia shifts within the fluid, and the subsequent stimulus is unbalanced with respect to the opposite ear, inappropriately causing symptoms of dizziness, spinning, and/or swaying.
  • #1 Benign paroxysmal positional vertigo – Wikipedia
    https://en.wikipedia.org/wiki/Benign_paroxysmal_positional_vertigo
    In rare cases, the crystals themselves can adhere to a semicircular canal cupula, rendering it heavier than the surrounding endolymph. Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles, thereby inducing an immediate and sustained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis. […] BPPV is one of the most common vestibular disorders in people presenting with dizziness; a migraine is implicated in idiopathic cases. Proposed mechanisms linking the two are genetic factors and vascular damage to the labyrinth. […] The inside of the ear is composed of an organ called the vestibular labyrinth. The vestibular labyrinth includes three semicircular canals, which contain fluids and fine hairlike sensors that act as a monitor to the rotations of the head. Other important structures in the inner ear includes the otolith organs, the utricle and saccule, that contain calcium carbonate crystals(otoconia) that are sensitive to gravity. […] The crystals may dislodge from the utricle (an otolith organ) and settle within the semicircular canals. When there is motion, the displaced otoconia shift within the endolymph of semicircular canals, causing an unbalanced (with respect to the opposite ear) stimulus, causing symptoms of BPPV.
  • #1
    https://step2.medbullets.com/ear-nose-throat/120131/benign-paroxysmal-positional-vertigo-bppv
    canalithiasis (calcium debris) within the semicircular canal leads to improper motion of the endolymph, which results in a spinning sensation […] most common site of canalithiasis is in the posterior semicircular canal […] inner ear sensory hair cells detects endolymph movement with head or body motion […] this causes the brain to perceive motion or position […] rotation acceleration is detected by the semicircular canals […] linear acceleration is detected by the utricle and saccule.
  • #1 Benign paroxysmal positional vertigo
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6383320/
    By comparison, the canalithiasis model cites freefloating particles within the lumen of the canal as the causal factor, a phenomenon that was first demonstrated in vivo by Parnes and McClure. […] Most cases of BPPV are idiopathic in origin and probably result from degeneration of the macula. Secondary causes of BPPV refer to identifiable causes of otoconial dislodgement. […] The posterior canal variant is by far the most common (80-90%) because it is the most gravity-dependent part of the vestibular labyrinth. […] The symptomatology of BPPV is a direct result of aberrant semicircular canal signalling which creates an illusory sense of motion.
  • #1 Benign Paroxysmal Positional Vertigo: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/884261-overview
    Although some controversy exists regarding the two pathophysiologic mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the entities actually coexist and account for different subspecies of BPPV. Canalithiasis (literally, „canal rocks”) is defined as the condition of particles residing in the canal portion of the SCCs (in contradistinction to the ampullary portion). These densities are considered to be free floating and mobile, causing vertigo by exerting a force. Conversely, cupulolithiasis (literally, „cupula rocks”) refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating. […] Particles in the canal slow and even reverse the movement of the cupula switch and create signals that are incongruous with the actual head movements. This mismatch of sensory information results in the sensation of vertigo.
  • #1 Benign Paroxysmal Positional Vertigo: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/884261-overview
    In 1962, Harold Schuknecht, MD, proposed the cupulolithiasis (heavy cupula) theory as an explanation for BPPV. […] In 1980, Epley published his theories regarding canalithiasis. He thought that the symptoms of BPPV were much more consistent with free-moving densities (canaliths) in the posterior SCC rather than fixed densities attached to the cupula. […] Canal densities would better explain the delay (latency), transient nystagmus, and reversal on return to upright than would cupular densities. This supports canalithiasis rather than cupulolithiasis as the mechanism for classic BPPV.
  • #1 :: JCN :: Journal of Clinical Neurology
    https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2010.6.2.51
    The detached otolith debris could be either attached to the cupula (cupulolithiasis) or may be free-floating in the semicircular canals (canalolithiasis). Pathological studies have shown that both of these conditions exist. The otolithic debris deflects the cupula and gives rise to a spinning sensation via a direct gravitational effect on the cupula or by inducing endolymph flow during head motion in the direction of gravity. According to the cupulolithiasis theory, a cupular deposit (heavy cupula) would induce a gravitational effect on the crista. However, the action of free-floating debris is the currently accepted pathophysiologic mechanism of typical BPPV. According to the canalolithiasis theory, the free-floating particles move under the influence of gravity when changing the position of the canal in the earth-vertical plane. The hydrodynamic drag of the particles induces endolymphatic flow, resulting in cupular displacement and leading to the observed typical responses.
  • #1 Benign paroxysmal positional vertigo
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6383320/
    Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular endorgan disease. This article aims to summarize research findings and key discoveries of BPPV. The pathophysiology, diagnosis, nonsurgical, and surgical management are discussed. […] Understanding the pathophysiology of both canalithiasis and cupulolithiasis has allowed for the development of various repositioning techniques. Of these, the particle repositioning maneuver is an effective way to treat posterior canal BPPV, the most common variant. […] The two prevailing theories regarding BPPV’s pathophysiology are the canalithiasis and cupulolithiasis models, and they differ with respect to how endolymphatic debris influences cupular dynamics. […] In the cupulolithiasis model, the particulate matter becomes adherent to the cupula itself. This cupular loading renders the system sensitive to gravitational forces, and the resulting alterations in cupular deflection lead to pathological perceptions of motion.
  • #1 Benign Paroxysmal Positional Vertigo (BPPV) – Vestibular Disorders Association
    https://vestibular.org/article/diagnosis-treatment/types-of-vestibular-disorders/benign-paroxysmal-positional-vertigo-bppv/
    Fluid in the semicircular canals does not normally react to gravity. However, the crystals do move with gravity, thereby moving the fluid when it normally would be still. When the fluid moves, nerve endings in the canal are excited and send a message to the brain that the head is moving, even though it isn’t. This false information does not match with what the other ear is sensing, with what the eyes are seeing, or with what the muscles and joints are doing, and this mismatched information is perceived by the brain as a spinning sensation, or vertigo, which normally lasts less than one minute. […] There are two types of BPPV: one where the loose crystals can move freely in the fluid of the canal (canalithiasis), and, more rarely, one where the crystals are thought to be hung up on the bundle of nerves that sense the fluid movement (cupulolithiasis). With canalithiasis, it takes less than a minute for the crystals to stop moving after a particular change in head position has triggered a spin. Once the crystals stop moving, the fluid movement settles and the nystagmus and vertigo stop. With cupulolithiasis, the crystals stuck on the bundle of sensory nerves will make the nystagmus and vertigo last longer, until the head is moved out of the offending position or the brain decides to suppress the noxious response. It is important to make this distinction, as the treatment is different for each variant.
  • #1 Geriatric benign paroxysmal positional vertigo: a single-center study | Brazilian Journal of Otorhinolaryngology
    https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-geriatric-benign-paroxysmal-positional-vertigo-S1808869423000459
    Benign Paroxysmal Positional Vertigo (BPPV) was more common in women. […] Geriatric BPPV patients often had risk factors associated with atherosclerosis. […] Horizontal canal-BPPV and multi-canal-BPPV were more common in geriatric patients. […] The effectiveness of canalith repositioning procedure may decrease with age. […] About 95% of cases of BPPV are idiopathic or degenerative, and aging and degenerative changes are responsible for the high incidence of BPPV in the elderly. […] With increasing age, there is a decrease in the amount of calcium carbonate crystals in the otoliths. This demineralization process weakens the fibrous connections between the otoliths, resulting in fissures or fragmentation, less stable otoliths, and dislodgement of otoconia in the utricles into the semicircular canals.
  • #1 BPPV — Benign Paroxysmal Positional Vertigo
    https://dizziness-and-balance.com/disorders/bppv/bppv.html
    BPPV is caused by crystals dislodged from the utricle of the inner ear. […] In Benign Paroxysmal Positional Vertigo (BPPV) dizziness and vertigo is triggered by particular positions because of debris which has collected within a part of the inner ear. […] Physically, BPPV results when the otoconia are dislodged from the utricle, become loose within the labyrinth, and fall backwards into one of the canals (usually the posterior). […] Otoconia may be dislodged due to wear/tear, trauma, disease. Usually it is blamed on wear/tear. […] In older people, the most common cause is degeneration of the vestibular system of the inner ear — „wear and tear” involving the otoliths. […] The most common cause of BPPV in people under age 50 is head injury. […] Between 8% and 20% of BPPV is attributed to trauma.
  • #1 Benign Paroxysmal Positional Vertigo – Ear, Nose, and Throat Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/ear-nose-and-throat-disorders/inner-ear-disorders/benign-paroxysmal-positional-vertigo
    BPPV is thought to be caused by displacement of otoconial crystals (calcium carbonate crystals normally embedded in the saccule and utricle). This displaced material stimulates hair cells most commonly in the posterior semicircular canal, occasionally in the lateral semicircular canal, and rarely in the superior semicircular canal, creating the illusion of motion. […] Etiologic factors include spontaneous degeneration of the utricular otolithic membranes, labyrinthine concussion, otitis media, ear surgery, recent viral infection (eg, viral neuronitis), head trauma, prolonged anesthesia or bed rest, previous vestibular disorders (eg, Meniere disease), and occlusion of the anterior vestibular artery. […] In BPPV, vertigo is caused by displacement of otoconial crystals into a semicircular canal; symptoms are triggered by head movement.
  • #1 Benign paroxysmal positional vertigo: Effective diagnosis and treatment | Cleveland Clinic Journal of Medicine
    https://www.ccjm.org/content/89/11/653
    Benign paroxysmal positional vertigo (BPPV), caused by wayward crystals (rocks) in the semicircular canals of the inner ear, is the most common cause of brief symptoms of vertigo secondary to head and body movements. […] BPPV is caused by free-floating otoconia that have been dislodged from the otolith organs as a result of injury, infection, diabetes, migraine, osteoporosis, prolonged bedrest, or aging. Dislodged otoconia can gather in the semicircular canals. Since each semicircular canal is oriented in a different plane in space, when the dislodged otoconia gather in 1 or more of them, they can be stimulated upon positional changes and cause vertigo and nystagmus. […] Most cases of BPPV are either idiopathic or caused by head trauma, but it can be a result of other vestibular disorders (eg, Menire disease, labyrinthitis) or central nervous system disorders (eg, migraine, multiple sclerosis). […] Recent evidence suggests BPPV has a seasonal aspect, perhaps related to varying vitamin D levels throughout the year. Otoconia are composed of calcium carbonate and therefore could have risk factors for demineralization, similar to bone.
  • #1 Benign Paroxysmal Positional Vertigo (BPPV) – Balance & Dizziness Canada
    https://balanceanddizziness.org/disorders/vestibular-disorders/bppv/
    Most cases of BPPV are idiopathic, meaning they happen for no apparent reason. […] Secondary BPPV can develop due to a range of conditions that cause damage to the inner ear and lead to crystals coming loose. […] Compared to idiopathic BPPV, secondary cases are more likely to affect both ears (bilateral), require more than one treatment and recur more frequently.
  • #1 BPPV — Benign Paroxysmal Positional Vertigo
    https://dizziness-and-balance.com/disorders/bppv/bppv.html
    There is also a strong association of BPPV with migraine. […] Viruses affecting the ear such as those causing vestibular neuritis and Meniere’s disease are significant causes. […] The combination of vestibular neuritis and BPPV is sometimes called Lindsay-Hemenway syndrome. […] BPPV has often been described as „self-limiting” because symptoms often subside or disappear within 1-2 months of onset. […] Loose otoconia are probably actively reabsorbed by the „dark cells” of the labyrinth. […] The Epley and Semont maneuvers, named after their inventors, are both intended to move debris or „ear rocks” out of the sensitive part of the ear (posterior canal) to a less sensitive location. […] The recurrence rate for BPPV after these maneuvers and resolution is about 22 percent at one year.
  • #1 BPPV — Benign Paroxysmal Positional Vertigo
    https://dizziness-and-balance.com/disorders/bppv/bppv.html
    BPPV often recurs. About 1/3 of patients have a recurrence in the first year after treatment, and by five years, about half of all patients have a recurrence. […] In some persons, the positional vertigo can be eliminated but imbalance persists. […] If cupulolithiasis of the posterior canal is suspected, it seems logical to treat with either the Epley with vibration, or alternatively, use the Semont maneuver. […] There are no controlled studies of cupulolithiasis to indicate which strategy is the most effective.
  • #1 Benign paroxysmal positional vertigo: a multi-center study | The Egyptian Journal of Otolaryngology | Full Text
    https://ejo.springeropen.com/articles/10.1186/s43163-022-00295-x
    Benign paroxysmal positional vertigo (BPPV) is believed to be attributed to dislodged otoliths from utricular macula into any of the semicircular canals, which results in canalithiasis, or cupulolithiasis, if otoliths adhere to the cupula of the semicircular canal. This results in bending and stimulation of the cupula and provoking vertigo and nystagmus in the plane of the affected canal. […] The time course of BPPV is characterized by spontaneous remissions that occur typically after days to weeks and recurrences that occur in about 50% of patients. […] BPPV is categorized according to its cause into primary which is usually idiopathic and secondary. The primary type is the commonest type. The chief causes of secondary BPPV are after ear surgery, trauma to the head, vestibular neuronitis, insufficient blood supply of the vestibulobassilar system, and metabolic disorders.
  • #1
    https://myhealth.alberta.ca/Health/pages/conditions.aspx?hwid=hw263714
    Benign paroxysmal positional vertigo (BPPV) is caused by a problem in the inner ear. Tiny calcium „stones” inside your inner ear help you keep your balance. When you have BPPV, these stones move into the semicircular canal in your inner ear where they can cause a feeling of spinning. […] When you move your head in certain ways, the stones in your semicircular canal move. Sensors in the semicircular canal are triggered by the stones, which causes a feeling of spinning. […] BPPV may go away in a few weeks by itself. If treatment is needed, it usually involves your doctor moving your head in different directions. Examples are Epley and Semont manoeuvres. These movements will move the particles out of the semicircular canals of your inner ear. […] Over time, your brain may react less and less to the confusing signals triggered by the particles in the inner ear. This is called compensation. It occurs fastest if you keep doing normal head movements, even if those movements cause the whirling feeling of vertigo.
  • #1 Benign Paroxysmal Positional Vertigo (BPPV) | Otolaryngology | Head and Neck Surgery
    https://ohns.ucsf.edu/balance-falls/BPPV
    One of the most common forms of vertigo, Benign Paroxysmal Positional Vertigo (BPPV) occurs when loose crystals from the one parts of the inner ear (the utricle) break off and end up in another part of the inner ear (typically the posterior semicircular canal). The crystals, aka otoconia, are composed of calcium carbonate, and help the utricle sense head tilt and acceleration by acting as a weight that will slide relative to the hair cells with head position changes. They can be displaced from the utricle for a variety of reasons, including aging, trauma, inflammation (neurititis), Menires disease, and surgery. Since the semicircular canals are designed to sense fluid movement (via the crista ampullaris) as part of their job in sensing head rotations, when the loose otoconia end up in the semicircular canals, they can mimic fluid movement, sending a false signal to the brain that you are moving quickly, when in reality you are not. This produces dizziness, nystagmus (rhythmic eye movement in same plane as the canal being stimulated), and nausea. Most cases involve the posterior semicircular canal, due to the fact that it is the most dependent portion of the inner ear (similar to why debris collects in the U-bend under a sink). However, the other two semicircular canals (the horizontal canal and the superior canal) can be affected as well, although this is much rarer. Treatment is aimed at moving the otoconia back into the vestibule, where it wont cause problems (and is likely reabsorbed but no one really knows). This is usually accomplished with the Epley maneuver for posterior canal BPPV, although occasionally other maneuvers (Semont, Brant-Daroff, Log Roll, Gufoni, etc.) are needed. Surgery can be considered in very rare cases where particle repositioning maneuvers are not effective, but this is very uncommon.
  • #1 Benign paroxysmal positional vertigo | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/benign-paroxysmal-positional-vertigo?lang=us
    Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo. It occurs secondary to change in posture and typically is associated with nystagmus. The etiology is thought to be due to changes of position of the otoliths in the inner ear, most commonly into the posterior semicircular canal. […] In benign paroxysmal positional vertigo, the otolithic crystals from the utricle and saccule become displaced and migrate into the semicircular canals, and when there is change in the static position of the head with respect to gravity, these otoliths move causing the fluid to also move when it ordinarily would not. This results in false signals to the brain causing a transient illusory sense of rotation (i.e. vertigo) until the head rests and the otoliths stop moving. […] The otoliths are most commonly displaced into the posterior semicircular canal (in up to 90% of cases), but can also less commonly affect the superior (anterior) canal, lateral (horizontal) canal, and even multiple canals at once. The presence of otoliths in the canals is often idiopathic, but can be secondary to head trauma or a residual effect of other vestibulopathies (e.g. Mnire disease, vestibular neuritis, etc.).
  • #1
    https://journals.lww.com/sjoh/fulltext/2022/24020/benign_paroxysmal_positional_vertigo_in_patients.1.aspx
    Benign paroxysmal positional vertigo (BPPV) is the most common type of peripheral vertigo. BPPV may be associated with Meniere’s disease (MD) and may be found at any stage of this disease. Hydropically induced damage to the maculae of the utricle and saccule or partial obstruction of the membranous labyrinth may be the cause for the coexistence of MD and BPPV. The pathophysiology of BPPV is the dislodgment of otoconia from the utricle. The otoconia are microscopic crystals of calcium carbonate which drift into the ampulla of the posterior semicircular canal, where these stimulate the end organ and trigger an attack of vertigo. BPPV may be associated with MD, and it may occur at any stage of this disease. The basic histopathological feature of MD is excessive endolymph in the endolymphatic sac, known as endolymphatic hydrops. The important theories for endolymphatic hydrops are viral infection, autoimmune involvement of the endolymphatic sac, a genetically determined abnormality for endolymph control, and variations in the position and size of the endolymphatic sac and its duct. Currently, it is thought that detached saccular otoconia are the causative factor for hydrops. The high prevalence of BPPV in MD patients could be explained by damage to the utricle caused by hydrops and subsequent otoconia detachment. Distension of the membranous labyrinth in MD can result in loss of its resilience, otolith detachment, and its partial obstruction. BPPV in MD often affects the horizontal SCC, and the predilection of horizontal SCC is because of development of otolithiasis in MD. Several authors have proposed that secondary BPPV has specific clinical characteristics which differ from those of idiopathic BPPV. The first difference is the longer duration of clinical manifestations. This may be due to either different pathogenetic mechanisms or treatment difficulties. Partial blockage of the posterior semicircular canal occurs by a dilated saccule which can cause adherence of otoliths to the membranous labyrinth in MD. Anatomical alterations of the labyrinth by hydrops probably are the important cause of the intractability of BPPV in MD.
  • #1 Benign Paroxysmal Positional Vertigo (BPPV) – Vestibular Disorders Association
    https://vestibular.org/article/diagnosis-treatment/types-of-vestibular-disorders/benign-paroxysmal-positional-vertigo-bppv/
    Benign Paroxysmal Positional Vertigo (or BPPV) is the most common cause of vertigo, which is a false sensation of motion, often reported as a spinning sensation. It occurs when calcium carbonate crystals (otoconia) that are normally embedded in gel in the utricle become dislodged and migrate into one or more of the three fluid-filled semicircular canals, where they are not supposed to be. […] BPPV is a mechanical problem in the inner ear. It occurs when some of the calcium carbonate crystals (otoconia) that are normally embedded in gel in the utricle become dislodged and migrate into one or more of the three fluid-filled semicircular canals, where they are not supposed to be. When enough of these particles accumulate in one of the canals, they interfere with the normal fluid movement that these canals use to sense head motion, causing the inner ear to send false signals to the brain.
  • #2 Benign paroxysmal positional vertigo
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6383320/
    Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular endorgan disease. This article aims to summarize research findings and key discoveries of BPPV. The pathophysiology, diagnosis, nonsurgical, and surgical management are discussed. […] Understanding the pathophysiology of both canalithiasis and cupulolithiasis has allowed for the development of various repositioning techniques. Of these, the particle repositioning maneuver is an effective way to treat posterior canal BPPV, the most common variant. […] The two prevailing theories regarding BPPV’s pathophysiology are the canalithiasis and cupulolithiasis models, and they differ with respect to how endolymphatic debris influences cupular dynamics. […] In the cupulolithiasis model, the particulate matter becomes adherent to the cupula itself. This cupular loading renders the system sensitive to gravitational forces, and the resulting alterations in cupular deflection lead to pathological perceptions of motion.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV): Treatment, Symptoms & Causes
    https://my.clevelandclinic.org/health/diseases/11858-benign-paroxysmal-positional-vertigo-bppv
    Benign paroxysmal positional vertigo (BPPV) is an inner ear disorder. BPPV can happen when otoconia (calcium carbonate particles) from the utricle get trapped in the semicircular canals of your inner ear. BPPV develops when calcium carbonate particles (otoconia) move into your semicircular canals (inner ear structures that control balance) and become trapped. Normally, the otoconia are part of your utricle, a vestibular organ next to your semicircular canals. In your utricle, the otoconia may become loose due to injury, infection or age. As your head position changes, the otoconia roll around and push on tiny hair-like structures (cilia) within your semicircular canals. Those cilia help transmit information about balance to your brain. Vertigo develops when the cilia are stimulated by the rolling otoconia.
  • #2 Benign Paroxysmal Positional Vertigo – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470308/
    Benign paroxysmal positional vertigo (BPPV) occurs due to the displacement of calcium-carbonate crystals or otoconia within the fluid-filled semicircular canals of the inner ear. […] Approximately 50% to 70% of BPPV cases occur with no known cause and are referred to as primary or idiopathic BPPV. […] The remaining cases are called secondary BPPV and are often associated with an underlying pathology, such as head trauma, vestibular neuronitis, labyrinthitis, Mnire disease, migraine, ischemia, and iatrogenic causes. […] With BPPV, otoconia (also known as „otoliths” or „canaliths”) dislodge and settle within the endolymph of the semicircular canals. […] When the head remains static, there is no stimulus. […] With motion, however, the displaced otoconia shifts within the fluid, and the subsequent stimulus is unbalanced with respect to the opposite ear, inappropriately causing symptoms of dizziness, spinning, and/or swaying.
  • #2 Benign Paroxysmal Positional Vertigo: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/791414-overview
    Benign paroxysmal positional vertigo (BPPV) is defined as an abnormal sensation of motion that is elicited by certain critical provocative positions. The provocative positions usually trigger specific eye movements (ie, nystagmus). The character and direction of the nystagmus are specific to the part of the inner ear affected and the pathophysiology. […] BPPV is a complex disorder to define; because an evolution has occurred in the understanding of its pathophysiology, an evolution has also occurred in its definition. […] Although some controversy exists regarding the two pathophysiologic mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the entities actually coexist and account for different subspecies of BPPV. Canalithiasis (literally, „canal rocks”) is defined as the condition of particles residing in the canal portion of the SCCs (in contradistinction to the ampullary portion). These densities are considered to be free floating and mobile, causing vertigo by exerting a force. Conversely, cupulolithiasis (literally, „cupula rocks”) refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.
  • #2 :: JCN :: Journal of Clinical Neurology
    https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2010.6.2.51
    Benign paroxysmal positional vertigo (BPPV) is characterized by brief recurrent episodes of vertigo triggered by changes in head position. BPPV is the most common etiology of recurrent vertigo and is caused by abnormal stimulation of the cupula by free-floating otoliths (canalolithiasis) or otoliths that have adhered to the cupula (cupulolithiasis) within any of the three semicircular canals. […] Schucknecht was the first to provide a pathophysiological concept of BPPV. In 1969 he proposed the theory of „cupulolithiasis” on the basis of pathological studies that demonstrated otolithic debris attached to the cupula. According to the theory, the cupula, which became heavy due to attached otolithic debris, could be deflected by position changes, thus evoking nystagmus. However, the concept of cupulolithiasis has several limitations and is thus unable to explain all of the characteristics of nystagmus and vertigo in BPPV. In 1979, Hall proposed the concept of „canalolithiasis”, which states that otolithic debris from the utricular macule migrates into the semicircular canal via the nonampullary portion, causing vertigo and nystagmus by moving freely inside the semicircular canal and inducing endolymph flow during positional changes. The concept of canalolithiasis was supported by the intraoperative observation of abundant free-floating debris in the endolymph of the posterior semicircular canal. This concept formed the theoretical basis of the canalith repositioning maneuvers (CRMs) to treat BPPV.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV) – Vestibular Disorders Association
    https://vestibular.org/article/diagnosis-treatment/types-of-vestibular-disorders/benign-paroxysmal-positional-vertigo-bppv/
    Fluid in the semicircular canals does not normally react to gravity. However, the crystals do move with gravity, thereby moving the fluid when it normally would be still. When the fluid moves, nerve endings in the canal are excited and send a message to the brain that the head is moving, even though it isn’t. This false information does not match with what the other ear is sensing, with what the eyes are seeing, or with what the muscles and joints are doing, and this mismatched information is perceived by the brain as a spinning sensation, or vertigo, which normally lasts less than one minute. […] There are two types of BPPV: one where the loose crystals can move freely in the fluid of the canal (canalithiasis), and, more rarely, one where the crystals are thought to be hung up on the bundle of nerves that sense the fluid movement (cupulolithiasis). With canalithiasis, it takes less than a minute for the crystals to stop moving after a particular change in head position has triggered a spin. Once the crystals stop moving, the fluid movement settles and the nystagmus and vertigo stop. With cupulolithiasis, the crystals stuck on the bundle of sensory nerves will make the nystagmus and vertigo last longer, until the head is moved out of the offending position or the brain decides to suppress the noxious response. It is important to make this distinction, as the treatment is different for each variant.
  • #2 Benign Paroxysmal Positional Vertigo: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/791414-overview
    Particles in the canal slow and even reverse the movement of the cupula switch and create signals that are incongruous with the actual head movements. This mismatch of sensory information results in the sensation of vertigo. […] In 1962, Harold Schuknecht, MD, proposed the cupulolithiasis (heavy cupula) theory as an explanation for BPPV. […] In 1980, Epley published his theories regarding canalithiasis. He thought that the symptoms of BPPV were much more consistent with free-moving densities (canaliths) in the posterior SCC rather than fixed densities attached to the cupula. […] Canal densities would better explain the delay (latency), transient nystagmus, and reversal on return to upright than would cupular densities. This supports canalithiasis rather than cupulolithiasis as the mechanism for classic BPPV.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV) for ophthalmologists – EyeWiki
    https://eyewiki.org/Benign_Paroxysmal_Positional_Vertigo_(BPPV)_for_ophthalmologists
    Benign paroxysmal positional vertigo (BPPV) is commonly attributed to calcium debris within the semicircular canals (SCC), which normally detect angular head accelerations. Debris in the SCC causes inappropriate endolymph movement with changes in position, and therefore causes the sensation of vertigo with positional movement. […] Two theories exist for the mechanism of action of BPPV. They differ with respect to how the debris influences cupular dynamics: Canalithiasis proposes that free-floating particles, otoconia, have moved from the utricle and collect near the cupula of the affected SCC. Gravity pulls the otoconia through the endolymph canal, creating a plunger-like effect which causes ipsidirectional cupular displacement. […] Cupulolithiasis proposes that the otoconial debris is attached to the cupula of the affected SCC instead of free-floating in the endolymph. Resulting alterations in cupular deflection lead to pathological perceptions of motion.
  • #2 Benign paroxysmal positional vertigo (BPPV) | Better Health Channel
    https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/benign-paroxysmal-positional-vertigo-bppv
    Benign paroxysmal positional vertigo (BPPV) occurs when crystals (called otoconia), normally located in one part of the vestibular (or balance) system of your inner ear (the utricle), become dislodged and collect in another part of the inner ear balance system (one of the semi-circular canals). […] BPPV is thought to be caused by little calcium carbonate crystals (otoconia) coming loose within the canals. Usually, these crystals are held in special reservoirs within other structures of the inner ear (utricle). It is thought that injury or degeneration of the utricle may allow the crystals to escape into the balance system and interfere with the fluid flow. […] There is also an association between BPPV and osteoporosis. However, in a large number of cases, there is no known cause.
  • #2 Benign paroxysmal positional vertigo: a multi-center study | The Egyptian Journal of Otolaryngology | Full Text
    https://ejo.springeropen.com/articles/10.1186/s43163-022-00295-x
    Benign paroxysmal positional vertigo (BPPV) is believed to be attributed to dislodged otoliths from utricular macula into any of the semicircular canals, which results in canalithiasis, or cupulolithiasis, if otoliths adhere to the cupula of the semicircular canal. This results in bending and stimulation of the cupula and provoking vertigo and nystagmus in the plane of the affected canal. […] The time course of BPPV is characterized by spontaneous remissions that occur typically after days to weeks and recurrences that occur in about 50% of patients. […] BPPV is categorized according to its cause into primary which is usually idiopathic and secondary. The primary type is the commonest type. The chief causes of secondary BPPV are after ear surgery, trauma to the head, vestibular neuronitis, insufficient blood supply of the vestibulobassilar system, and metabolic disorders.
  • #2 Benign paroxysmal positional vertigo (BPPV) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/vertigo/symptoms-causes/syc-20370055
    Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo the sudden sensation that you’re spinning or that the inside of your head is spinning. […] BPPV is often associated with a minor to severe blow to your head. Less common causes of BPPV include disorders that damage your inner ear or, rarely, damage that occurs during ear surgery or long periods positioned on your back, such as in a dentist chair. BPPV also has been associated with migraines. […] For many reasons, these crystals can become dislodged. When they become dislodged, they can move into one of the semicircular canals especially while you’re lying down. This causes the semicircular canal to become sensitive to head position changes it would normally not respond to, which is what makes you feel dizzy.
  • #2 Benign Paroxysmal Positional Vertigo – Ear, Nose, and Throat Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/ear-nose-and-throat-disorders/inner-ear-disorders/benign-paroxysmal-positional-vertigo
    BPPV is thought to be caused by displacement of otoconial crystals (calcium carbonate crystals normally embedded in the saccule and utricle). This displaced material stimulates hair cells most commonly in the posterior semicircular canal, occasionally in the lateral semicircular canal, and rarely in the superior semicircular canal, creating the illusion of motion. […] Etiologic factors include spontaneous degeneration of the utricular otolithic membranes, labyrinthine concussion, otitis media, ear surgery, recent viral infection (eg, viral neuronitis), head trauma, prolonged anesthesia or bed rest, previous vestibular disorders (eg, Meniere disease), and occlusion of the anterior vestibular artery. […] In BPPV, vertigo is caused by displacement of otoconial crystals into a semicircular canal; symptoms are triggered by head movement.
  • #2 BPPV — Benign Paroxysmal Positional Vertigo
    https://dizziness-and-balance.com/disorders/bppv/bppv.html
    There is also a strong association of BPPV with migraine. […] Viruses affecting the ear such as those causing vestibular neuritis and Meniere’s disease are significant causes. […] The combination of vestibular neuritis and BPPV is sometimes called Lindsay-Hemenway syndrome. […] BPPV has often been described as „self-limiting” because symptoms often subside or disappear within 1-2 months of onset. […] Loose otoconia are probably actively reabsorbed by the „dark cells” of the labyrinth. […] The Epley and Semont maneuvers, named after their inventors, are both intended to move debris or „ear rocks” out of the sensitive part of the ear (posterior canal) to a less sensitive location. […] The recurrence rate for BPPV after these maneuvers and resolution is about 22 percent at one year.
  • #2 Vertigo Treatment in Joliet, New Lenox and Morris, Illinois
    https://www.entsurgicalillinois.com/vertigo.html
    In Benign Paroxysmal Positional Vertigo (BPPV) dizziness is generally thought to be due to debris which has collected within a part of the inner ear. This debris can be thought of as „ear rocks”, although the formal name is „otoconia”. Ear rocks are small crystals of calcium carbonate derived from a structure in the ear called the „utricle”. The utricle may have been damaged by head injury, infection, or other disorder of the inner ear, or may have degenerated because of advanced age. In older people, the most common cause is degeneration of the vestibular system of the inner ear. BPPV becomes much more common with advancing age. In half of all cases, BPPV is called „idiopathic,” which means it occurs for no known reason. Viruses affecting the ear such as those causing vestibular neuritis, minor strokes such as those involving anterior inferior cerebellar artery (AICA) syndrome, and Meniere’s disease are significant but unusual causes. Occasionally BPPV follows surgery, where the cause is felt to be a combination of a prolonged period of supine positioning, or ear trauma when the surgery is to the inner ear. BPPV is also common in persons who have been treated with ototoxic medications such as gentamicin. There are several rarer variants of BPPV which may occur spontaneously as well as after the Brandt-Daroff maneuvers or Epley/Semont maneuvers. They are mainly thought to be caused by migration of otoconial debris into canals other than the posterior canal, the anterior or lateral canal. Cupulolithiasis is a condition in which debris is stuck to the cupula of a semicircular canal, rather than being loose within the canal. The mechanistic hypothesis is based on pathological findings of deposits on the cupula made by Schuknecht and Ruby in three patients who had BPPV during their lives. Vestibulolithiasis is a hypothetical condition in which debris is present on the vestibule-side of the cupula, rather than being on the canal side. For the vestibulolithiasis mechanism, when the head is moved, stones or other debris might shift from vestibule to ampulla, or within the ampulla, impacting the cupula. If debris can get into one canal, why shouldn’t it be able to get into more than one? It is common to find small amounts of horizontal nystagmus or contralateral downbeating nystagmus in a person with classic posterior canal BPPV.
  • #2
    https://link.springer.com/article/10.1007/s00415-020-10314-7
    Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo worldwide. […] This review considers recent advances in the diagnosis and management of BPPV including the use of web-based technology and artificial intelligence as well as the evidence supporting the use of vitamin D supplements for patients with BPPV and subnormal serum vitamin D. […] Decreased serum vitamin D in idiopathic benign paroxysmal positional vertigo. […] Prevention of benign paroxysmal positional vertigo with vit D supplementation: a randomized trial. […] Prevention of recurrent benign paroxysmal positional vertigo with vitamin D supplementation: a meta-analysis. […] Otolith dysfunction in recurrent benign paroxysmal positional vertigo after mild traumatic brain injury. […] The effects of the vestibular rehabilitation on the benign paroxysmal positional vertigo recurrence rate in patients with otolith dysfunction.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV): Causes, Symptoms, and Treatment Options
    https://www.houstonent.com/blog/benign-paroxysmal-positional-vertigo-bppv-causes-symptoms-and-treatment-options
    This false information doesn’t match what your other ear is sensing, with what your joints and muscles are doing and what your eyes are seeing and your brain perceives the mismatched information as vertigo, or a spinning sensation. This usually lasts for only a minute. Some individuals feel symptom-free between vertigo spells, while other people may feel a mild sense of disequilibrium or imbalance.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV) | HealthLink BC
    https://www.healthlinkbc.ca/healthwise/benign-paroxysmal-positional-vertigo-bppv
    Benign paroxysmal positional vertigo (BPPV) is caused by a problem in the inner ear. Tiny calcium „stones” inside your inner ear help you keep your balance. When you have BPPV, these stones move into the semicircular canal in your inner ear where they can cause a feeling of spinning. […] When you move your head in certain ways, the stones in your semicircular canal move. Sensors in the semicircular canal are triggered by the stones, which causes a feeling of spinning. […] Over time, your brain may react less and less to the confusing signals triggered by the particles in the inner ear. This is called compensation. It occurs fastest if you keep doing normal head movements, even if those movements cause the whirling feeling of vertigo.
  • #2 Benign paroxysmal positional vertigo | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/benign-paroxysmal-positional-vertigo?lang=us
    Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo. It occurs secondary to change in posture and typically is associated with nystagmus. The etiology is thought to be due to changes of position of the otoliths in the inner ear, most commonly into the posterior semicircular canal. […] In benign paroxysmal positional vertigo, the otolithic crystals from the utricle and saccule become displaced and migrate into the semicircular canals, and when there is change in the static position of the head with respect to gravity, these otoliths move causing the fluid to also move when it ordinarily would not. This results in false signals to the brain causing a transient illusory sense of rotation (i.e. vertigo) until the head rests and the otoliths stop moving. […] The otoliths are most commonly displaced into the posterior semicircular canal (in up to 90% of cases), but can also less commonly affect the superior (anterior) canal, lateral (horizontal) canal, and even multiple canals at once. The presence of otoliths in the canals is often idiopathic, but can be secondary to head trauma or a residual effect of other vestibulopathies (e.g. Mnire disease, vestibular neuritis, etc.).
  • #2 Benign Paroxysmal Positional Vertigo (BPPV): Causes, Symptoms, and Treatment Options
    https://www.houstonent.com/blog/benign-paroxysmal-positional-vertigo-bppv-causes-symptoms-and-treatment-options
    Benign paroxysmal positional vertigo is a mechanical issue in your inner ear. The most common BPPV causes revolve around the crystals in your ear. It occurs when you have some of the (calcium carbonate crystals, otoconia that are usually embedded in the utricle (the larger of the cavities filled with fluid and form part of your inner ear labyrinth) gel and become dislodged, migrating into one or more of your three fluid-filled semicircular canals (bony inner ear channels), where they shouldn’t be. […] When you have too many of these particles accumulating in one of your canals, they impact the regular fluid movement your canals use for sensing head motion and cause your inner ear to send your brain false signals. Semicircular canal fluid doesn’t usually react to gravity. But, the crystals move with gravity which moves the fluid when it would usually be still. As the fluid moves, your canal nerve endings are excited and start sending your brain a message your head is moving, even when it’s not.
  • #2 Benign Paroxysmal Positional Vertigo (BPPV): Treatment, Symptoms & Causes
    https://my.clevelandclinic.org/health/diseases/11858-benign-paroxysmal-positional-vertigo-bppv
    The most effective benign paroxysmal positional vertigo treatments involve physical therapy exercises. The goal of these exercises is to move the calcium carbonate particles out of your semicircular canals and back into your utricle. Here, the particles resorb more easily and dont cause uncomfortable symptoms. […] BPPV exercises sometimes called canalith repositioning procedures typically take about 15 minutes to complete. Particle repositioning involves a series of physical movements that change the position of your head and body. These actions shift the otoconia out of your semicircular canals and back into their proper location in your utricle.
  • #3 Benign paroxysmal positional vertigo | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/benign-paroxysmal-positional-vertigo?lang=us
    Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo. It occurs secondary to change in posture and typically is associated with nystagmus. The etiology is thought to be due to changes of position of the otoliths in the inner ear, most commonly into the posterior semicircular canal. […] In benign paroxysmal positional vertigo, the otolithic crystals from the utricle and saccule become displaced and migrate into the semicircular canals, and when there is change in the static position of the head with respect to gravity, these otoliths move causing the fluid to also move when it ordinarily would not. This results in false signals to the brain causing a transient illusory sense of rotation (i.e. vertigo) until the head rests and the otoliths stop moving. […] The otoliths are most commonly displaced into the posterior semicircular canal (in up to 90% of cases), but can also less commonly affect the superior (anterior) canal, lateral (horizontal) canal, and even multiple canals at once. The presence of otoliths in the canals is often idiopathic, but can be secondary to head trauma or a residual effect of other vestibulopathies (e.g. Mnire disease, vestibular neuritis, etc.).