Fig. 5. Acute unilateral loss of semicircular canal function causing vestibular nystagmus. A. Disruption of the left superior division of the VIIIth nerve from vestibular neuritis. Loss of spontaneous neural activity from the left side causes slow phases to the left from relative excitation of the right horizontal semicircular canal (HC). B. Features of nystagmus. By convention, right eye position is up and left eye position is down. As the eyes move across the orbit, a quick phase resets the eyes back to the right. Quick phases are generated by burst cells, which are not part of the vestibular system. Nystagmus is labeled according to the direction of the quick phases. Consequently, this would be called a right-beating nystagmus. The lesion also disrupts spontaneous neural activity from the left anterior semicircular canal (AC), which results in right torsional nystagmus (the superior pole of each eye beats right). The intensity of nystagmus increases when the patient looks in the direction of the quick phases (B, bottom). If fixation is blocked by Frenzel glasses, nystagmus also increases and is seen clearly even in primary gaze (B, top).