depression and extorsion of the other eye [6, 47]. During the next half-cycle, there is a reversal of the vertical and torsional movements. The frequency is lower in the pendular (2–4 Hz) than in the jerk variety.

Etiology

Jerk hemi-seesaw nystagmus has been attributed to unilateral mesodiencephalic lesions [48], which affect the interstitial nucleus of Cajal and its vestibular afferents from the vertical semicircular canals [49]. The pendular form is associated with lesions that affect the optic chiasm; it can be congenital. Loss of crossed visual input seems to be the crucial element in the pathophysiology of pendular seesaw nystagmus [50].

Therapeutic Recommendations

Alcohol was reported to have a beneficial effect (1.2 g/kg body weight) in 2 patients [51, 52], as does clonazepam [1]. More recently, Averbuch-Heller reported on 3 patients with a seesaw component to their pendular nystagmus, who improved with gabapentin [53].

Periodic Alternating Nystagmus

Clinical Aspects

Periodic alternating nystagmus is a spontaneous horizontal beating nystagmus which periodically changes direction after 100–240 s [6]. Consequently, the patients complain of increasing/decreasing oscillopsia. When the nystagmus amplitude gradually decreases, the nystagmus reverses its direction, and then the amplitude increases again. Periodic alternating nystagmus also disrupts visual fixation. During the nystagmus, patients often complain of increasing/ decreasing oscillopsia [11].

Etiology

Animal and human experiments show that the disinhibition of the GABAergic velocity-storage mechanism, which is mediated by the vestibular nuclei, is responsible for the nystagmus [54, 55]. Patients with periodic alternating nystagmus commonly have vestibulocerebellar lesions or, very rarely, intoxications [56, 57]. The underlying etiologies are craniocervical anomalies, multiple sclerosis, cerebellar degenerations or tumors, anticonvulsant therapy, and bilateral visual loss. Recently, autoantibodies directed against glutamic acid decarboxylase were described in a patient with progressive cerebellar ataxia and periodic alternating nystagmus, suggesting an autoimmune mechanism [58].