Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder, accounting for more than 20% of all hospital visits for dizziness and vertigo. BPPV is a mechanical labyrinthine disorder, due to detached utricular otoconia debris displaced within the semicircular canals, free-floating within the canal lumen or attached to the ampullary cupula. It is characterized by recurrent vertigo triggered by changing head position with respect to gravity. BPPV is a mechanical disorder, therefore its therapy is mainly physical, and over the years, several maneuvers have been proposed for the treatment of each canal. Despite the wide range of treatment techniques available, well tolerated and promptly effective maneuvers should be preferred, step by step adapted to each case, in order to minimize patient’s discomfort. The “minimum stimulus strategy” (MSS) is the response to a minimal invasive approach. In fact, it is a nystagmus-based approach aimed to reduce the number of diagnostic and therapeutic maneuvers required for BPPV management. This type of approach, initially applied by Epley to the posterior canal, has been subsequently extended to the treatment of the other variants of BPPV. In fact, in 2003, it was proposed to begin the BPPV examination already in the sitting position, observing the nystagmus induced and/or modified by the upright head pitch test (uHPT), bending the patient’s head forward and backward in the pitch plane around the Y-axis. Even more recently, the approach in the sitting position has been enriched with other tests, rotating the patient’s head in other planes: the roll plane along the X-axis by the upright head roll test (uHRT), and two additional planes aligned with each couple of vertical semicircular canals, the left anterior/right posterior (LARP) plane, the upright LARP test (uLARP), and the right anterior/left posterior (RALP) plane, the upright RALP test (uRALP). All these tests have been defined “Upright BPPV Protocol” (UBP), it consists of slowly rotating the patient’s head along all the semicircular canals’ planes while sitting, simultaneously monitoring the evoked nystagmus by video-Frenzel goggles. Another point of great interest for scientific research in recent years has been the role played by vitamin D deficiency in BPPV. Indeed, vitamin D deficiency may induce BPPV by several mechanisms, having both direct “primary otolithic” (calcium-mediated) effects and indirect “secondary labyrinthine” (vessel-mediated) effects. In addition, another phenomenon has attracted the attention of researchers in BPPV pathophysiology, which is the oxidative stress. The latter is able to modify calcium homeostasis and to induce endothelial damage, thus enhancing the effects of vitamin D deficiency in BPPV onset and recurrence. So, vitamin D and anti-oxidative agents may have a synergic and complementary action in reducing BPPV relapses as well as post-manoeuver residual dizziness. The aim of this chapter is to shed light on all of these new aspects about BPPV pathophysiology and its management.