Table 1.

Publications Examining the Presence of Debris in the Labyrinth Microscopically or Macroscopically in the Literature

Author	Year	Study Design	Number of Patients	Age of Patient	Findings (Microscopic or Macroscopic)	BPPV Symptomatology	Comment of Authors
Dix–Hallpike	1952	Case report-histologic study	1 case	40	Normal appearing SCCs, severe degeneration in utriculus, sacculus and cochlea, degenerating sensory epithelium of utriculus, stroma thickened and infiltrated with cells, missing in otolithic membrane	Severe BPPV
Lindsay–Hemenway	1956	Case report-histologic study	1 case	78	Degeneration in part of superior vestibular nerve, ampulla of posterior SCC protected, missing in utricular otolithic membrane	Severe BPPV	Vascular occlusion supplying the anterior vestibular labyrinth
Cawthorne–Hallpike	1957	Case report-histologic study	1 case	59	Severe degeneration in utricular macula, severe degeneration in lateral SCC crista and nerve posterior SCC and crista protected	Severe BPPV	Impaired arterial support due to atheromatous occlusion
Schuknecht	1969	Case report-histologic study	2 cases	68-77	Case 1: basophilic homogenous deposits in the posterior part of posterior SCC cupula Case 2: granular basophilic stained deposits on the membranous wall in the most inferior part of the posterior SCC and attached to the posterior SCC cupula	Paroxysmal positional vertigo	Deposits arise from degenerate inner ear structures
Schuknecht-Ruby	1973	Case report-histologic study Temporal bone histologic study	1 case, 391 temporal bones	87	Case: dense basophilic deposits in the posterior SCC cupula TB: deposits in SCCs in 149 temporal bones (38%)	No vertiginous symptom	Due to postmortem degeneration
Parnes-McClure	1992	Case report-macroscopic examination	2 cases	81-84	Posterior canal occlusion was performed in 21 ears with resistant BPPV, only 2 patients had floating particles in the posterior SCC (the oldest patients in the study)	Resistant BPPV	Particles due to degenerative changes in the inner ear
Moriatry	1992	Temporal bone-histologic study	560 Temporal bones		22% of SCCs have basophilic granular deposits in their cupula, there are microfractures in the otic capsule.	No history of BPPV	Debris is formed because of small hemorrhages due to microfractures.
Kveton	1994	Macroscopic examination	10 cases		9 out of 10 patients operated for acoustic tumor have particles in the membranous labyrinth.	Only 1 patient had preoperative vertigo	Particles may be normal findings.
Naganuma	1996	Temporal bone-histologic study	87 Temporal bones		Basophilic deposit detected in 62% of SCCs, deposits increase with age.	55% of patients have no complaints with the labyrinth.	Otolith presence in SCCs is common but mostly asymptomatic.
Welling	1997	Macroscopic study	99 cases		Translabyrinthine acoustic tumor excision or labyrinthectomy was performed in 73 patients without BPPV, no particles were detected in any of them. Posterior SCC occlusion was performed in 26 patients with BPPV, and particles were detected in only 8.		Degeneration due to age
Bachor	2002	Temporal bone-histologic study	121 cases		186 TB studied, the rate of deposits in SCC cupulae 35/276 (12.7%)		Deposits are result of aging labyrinth
Gacek	2003	Temporal bone-histologic study	5 cases		There is no deposit in 4 TBs, 50% loss of ganglion cells in the superior vestibular part in all, loss of neurons in the inferior vestibular part; 50% in 3 TB and 30% in 2 TB	History of BPPV	BPPV occurs with the loss of inhibitory effect of otolith organs on SCCs.
Kusunoki	2005	Temporal bone-histologic study	23 Temporal bones		All received aminoglycoside treatment within 6 months prior to death, 34.8% basophilic material available in SCCs.	No history of BPPV	Basophilic material due to ototoxicity
Kao	2017	Case report-macroscopic examination	2 cases	59-70	Posterior SCC occlusion was applied, particle detected.	Severe BPPV	Particles are intact and degenerated otoliths separated from the otolithic membrane.

BPPV, benign paroxysmal positional vertigo; SCC, semicircular canal; TB, temporal bone.