“…Ataxia results from dysfunction of the cerebellum, or cerebellar inflow / outflow tracts within the pons, midbrain, and thalamus. Opsoclonus is thought to originate from either the cerebellum (Wong et al, 2001) or dysfunction of omnipause neurons in the pons (Kim et al, 2007; Ramat et al, 2008). As there is a minimal brain inflammation in OMAS (Kilgo and Schwartze, 1984), autoantibodies in OMAS may directly bind to their target antigen, disrupting its function without causing significant inflammatory tissue destruction, analogous to what is seen in encephalidities associated with known neuronal surface antigens (Bien et al, 2012; Dalmau et al, 2007).…”