Background: Saccades are essential for optimal visual function. Chiari type I I malformation (CII) is a congenital anomaly of the cerebellum and brainstem, as sociated with spina bifida. Objective: To investigate the effects of CII on sacc ades and correlate saccadic parameters with brain MRI measurements. Methods: Sac cades were recorded in 21 participants with CII, aged 8 to 19, using an infrared eye tracker. Thirty- nine typically developing children served as controls. Pa rticipants made saccades to horizontal and vertical target steps. Nineteen parti cipants with CII had MRI. Regression analyses were used to investigate the effec ts of spinal lesion level, number of shunt revisions, presence of nystagmus, and midsagittal MRI measurements on saccades. Results: Saccadic amplitude gains, as ymptotic peak velocities, and latencies did not differ between the control and C II groups (p > 0.01). No significant differences were found between saccadic gai ns, asymptotic peak velocities or latencies, and spinal lesion level, number of shunt revisions, presence of nystagmus, or MRI measurements. Conclusions: Saccad es were normal in most participants with Chiari Ⅱ malformation (CII). Neural c oding of saccades is robust and is typically not affected by the anatomic deform ity of CII. Background: Saccades are essential for optimal visual function. Chiari type II malformation (CII) is a congenital anomaly of the cerebellum and brainstem, as sociated with spina bifida. Objective: To investigate the effects of CII on sacc ades and correlate saccadic parameters with brain MRI measurements. Methods: Sac cades were recorded in 21 participants with CII, aged 8 to 19, using an infrared eye tracker. Pa rticipants made saccades to horizontal and vertical target steps. Nineteen parti cipants with CII had MRI. Regression analyzes were used to investigate the effector ts of spinal lesion levels, number of shunt revisions, presence of nystagmus, and midsagittal MRI measurements on saccades. Results: Saccadic amplitude gains, as ymptotic peak velocities, and latencies did not differ between the control and C II groups (p> 0.01). No significant differences were found between saccadic gai ns, asymptotic peak velocities or Conclusions: Saccad es were normal in most participants with Chiari II malformation (CII). Neural coding of saccades is robust and is typically not affected by the anatomic deform ity of CII.