Background/Objectives: Spontaneous-reversing positional nystagmus (SRPN) represents an atypical positional nystagmus in benign paroxysmal positional vertigo (BPPV) as it spontaneously reverses its direction in the same position. The inversion of nystagmus has been related to different pathomechanisms including rebound cupular deflections, peripheral/central short-term adaptation mechanisms of the vestibulo-ocular reflex (VOR) and coexistence of canalolithiasis and cupulolithiasis. Though it has been mainly described in lateral semicircular canal BPPV, SRPN can also occur in case of posterior semicircular canal (PSC) involvement when paroxysmal positional upbeating nystagmus (pPUBN) with ipsilesional torsional components is followed by positional downbeating nystagmus (pDBN) with contralesional torsional components in Dix-Hallpike test (DHT). Recently, the use of the video-head impulse test (vHIT) has been recommended in the differential diagnosis of BPPV with pDBN (anterior semicircular canal-BPPV versus non-ampullary PSC-BPPV) as it can detect endolymphatic flow dysfunctions due to an incomplete canalith jam. This study aims to provide possible etiopathogenetic hypotheses to explain SRPN in PSC-BPPV assuming that patients exhibiting reduced VOR-gain values for the affected PSC could have an additional otolith clot in the non-ampullary arm of the canal. Methods: The records of 42 patients (5 males, 37 females, mean age 68.4 ± 11.2 years) with PSC-BPPV exhibiting SRPN were retrospectively reviewed, including recent history of previous BPPV, nystagmus duration, presence of pDBN in contralateral DHT, VOR-gain values at the vHIT and the outcome of canalith repositioning maneuvers (CRM). Results: Patients with reduced PSC VOR-gain (62% of cases) exhibited higher rate of previous ipsilateral/bilateral PSC-BPPV (p<0.05), shorter first-phase pPUBN (p<0.01), higher incidence of pDBN in contralateral DHT (p<0.001) and lower success rate of CRM (p<0.05) compared to the patients with normal PSC VOR-gain. PSC-VOR gain normalized in most cases with impaired values after symptoms resolution (p<0.001). Conclusions: In a consistent group of patients with PSC-BPPV and SRPN, the second-phase pDBN could be likely explained by the coexistence of an additional clot of debris partially entrapped in the non-ampullary arm of the PSC. Compared to the condition with a single clot free to float in the ampullary arm of the involved PSC, this novel scenario consistent with two simultaneous clumps of otoliths within different PSC arms could likely result in weaker first-phase pPUBN, detection of pDBN in bilateral DHT and in a transient PSC VOR-gain impairment, along with preventing an easy otolith reposition with CRM