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Benign paroxysmal positional vertigo (BPPV) is the most common type of vertigo, caused by otoconia falling from the utricle into a semicircular canal (SCC). After successful repositioning maneuvers residual dizziness (RD) has been described and several reasons are used to explain RD. It can last for only a few days or weeks, but also much longer. We present a patient with a severe traumatic loss of otoconia from both maculae utriculi and a persistent imbalance more than 9 years. We think that the loss of otoconia from the utricular and probably also saccular macula induced a sudden reduction of her ability to sense gravity thus logically explaining her symptoms. We show the vestibular test results also supporting our hypothesis and we extrapolate this support to other forms of so far unexplained dizziness especially increasing imbalance with aging. We also discuss the normal c- and oVEMP indicating intact haircell function and supporting our hypothesis of isolated otoconial loss as the major cause for imbalance.

Objective To determine whether patients with acute unilateral peripheral vestibulopathy (PVP), often called "vestibular neuritis/neuronitis or neuropathy" (VN) have a vestibular lesion pattern consistent with the distribution of the neurological afferents. Background Much is known about the clinical nature of PVP, however less so about its etiology and pathogenesis. Due to the frequency with which VN is used to describe the syndrome, an inflammation of the vestibular nerve or of one of its branches is often assumed to be the cause of PVP, though there is insufficient data so far to support this assumption. Methods We conducted a retrospective study of 25 patients who had presented to our clinic with PVP and had all vestibular receptor organs tested shortly after start of symptoms. We analysed their vestibular lesion patterns in order to determine whether they were consistent with the neuritis hypothesis (NH). Results The lesion patterns varied conspicuously. 76% did not follow an innervation pattern, thereby contradicting the NH and only 24% had a lesion pattern that either definitely (16%) or probably (8%) supported the NH. Conclusion These results should remind us to be careful before jumping to quick conclusions about the pathogenetic nature of PVP. With any reason to question VN as the only cause of PVP, we should reconsider the treatment approach to PVP. If the cause probably or even possibly lies inside the vestibular labyrinth, an intratympanic steroid injection might prove to be a more effective measure, even in first-line treatment. If the etiology is unsure, a combination of systemic and intratympanic steroid treatment may be adequate.