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Adaptive Control of Saccades in Children with Dancing Eye Syndrome

Dancing eye syndrome (DES), or opsoclonus-myoclonus, is a rare neurological syndrome characterized by opsoclonus (spontaneous chaotic involuntary bursts of back-to-back saccades in all directions) and myoclonus (jerky involuntary movements of the limbs). Onset is usually in childhood, under 3 years of age. Although there can be good recovery from the acute symptoms, long-term neurological sequelae are often found.1,2 The etiology of DES is as yet unknown and may involve the brainstem and/or the cerebellum. A recent SPECT study of two children with DES has implicated the vermis of the cerebellum, in particular with the generation of opsoclonus.3 Shawkat et al. (1993) reported that visually guided reflexive saccades recorded from DES patients during the acute phase of their disease are hypermetric (gain >1).4 Saccadic dysmetria in humans is often associated with lesions of the vermis of the cerebellum and/or the deep cerebellar nuclei.5–7 Saccadic gain is under adaptive control (AC), which maintains the optimal accuracy of saccades with respect to their target, and it has been shown experimentally that the vermis of the cerebellum and fastigial nuclei in monkeys are necessary for AC.8 Given possible neuropathology in the cerebellum, and specifically the vermis, it is plausible that patients with DES may have chronic saccade dysmetria consistent with the failure of the saccadic AC system. We set out to test this hypothesis in a group of children and young adults with DES. A gain-decreasing intra-saccadic target perturbation paradigm was used to test the active functioning of the AC system.