The case report by Hyun-Ah et al. [1] (in this issue) describes a quite uncommon condition, the rotational vertebral artery syndrome (RVAS), and it is worth reading. The vestibular system is an environment in which many neurologists feel uncomfortable, but this report shows how the knowledge of vestibular physiology, a careful observation and a little instrumental support may elucidate the pathophysiology of the signs and drive to the diagnosis. RVAS consists of recurrent short spells of rotatory vertigo triggered after a few seconds of head rotation that causes a labyrinthine ischemia because of the compression of a dominant vertebral artery. Brief spells of vertigo induced by head rotation are very likely to be a benign paroxysmal positional vertigo (BPPV), but BPPV was ruled out by the features of nystagmus, which did not fit the mixed up-beat and torsional nystagmus induced by the Dix–Hallpike maneuver in posterior canal BPPV, or the geotropic (or apogeotropic) nystagmus induced by the Mc Clure maneuver in the lateral canal BPPV. Color duplex sonography of the vertebral arteries may show a significant unilateral blood flow reduction during head rotation, but this usually has no consequences because of the suppliance by collateral vessels. However, if a vertebral artery is clearly dominant and the circulation from collateral vessel is ineffective to compensate for an abrupt blood flow reduction, an external compression may cause a symptomatic transient ischemia. The pattern of signs and symptoms is not stereotyped, and in those two patients were suggestive for RVAS. In neurology, ischemia usually corresponds to a deficit, a loss of function. This rule of thumb was not applicable to the two patients: the physiology of the vestibular system [2] tells us that the features of their nystagmus could only be explained by an excitation rather than by an inhibition of the labyrinth ipsilateral to the vertebral artery that proved to be compressed by contralateral head rotation. However, the two mechanisms, inhibition and excitation, can be reconciled if we make a step further and consider the physiology of the vestibular system at a cellular level. The apical surface of vestibular hair cells (the vestibular receptors) faces the endolymph, a fluid with a high concentration of potassium, whereas the baso-lateral surface is surrounded by perilymph, a fluid with a low concentration of potassium. The dark cells are important to guarantee the homeostasis of inner ear fluids, including the flow of potassium from the perilymph to the endolymph by an Na–K–ATPase mechanism [3]; a few seconds of ischemia triggers a uabain-like blockade of the Na–K– ATPase mechanism, and the dark cells are no longer able to prevent the increase of potassium concentration in the perilymph. It has been demonstrated that during sinusoidal cupula deflection, the perilymph potassium content increases during excitatory half-periods and decreases during inhibitory half-periods [3]. Accordingly, an increase in perilymph potassium concentration results in increased hair cells activity. To summarize from a cellular stand point: ischemia after a few seconds is responsible for a loss of function of dark cells, with an increase of potassium in the perilymph that causes an activation of hair cells, and hence the appearance M. Versino (&) S. Colnaghi Laboratorio Neuro-otologia e Neuro-Oftalmologia, Brain Connectivity Centre, Fondazione Istituto Neurologico Nazionale C Mondino, IRCCS, Pavia, Italy e-mail: maurizio.versino@unipv.it