The vestibular system provides us with reflexive responses of eye movements and balance control, as well as with perceptual estimates of self-motion and gravity direction. Crucial to its proper functioning is a bilaterally balanced vestibular signal originating from the vestibular end organs in the inner ears and projecting via vestibular nerve afferents to the brainstem vestibular nuclei. Disturbances of the bilateral vestibular interplay become evident in cases of acute unilateral peripheral vestibular deafferentation. The resultant sudden imbalance of vestibular afferent tone at the level of the vestibular nuclei leads to pronounced ocular–motor and postural impairment, as well as to intensive vertigo and/or dizziness, accompanied by autonomic symptoms, such as nausea and vomiting. Subsequent compensatory mechanisms efficiently diminish these static symptoms (such as spontaneous nystagmus) within days and allow functional recovery of dynamic symptoms (such as blurred vision during fast head turns) to such a degree that most patients return to their normal daily activities within weeks. This article aims to provide an understanding about the pathophysiological changes after unilateral vestibular deafferentation and the current knowledge on the compensatory mechanisms.