Saccades are fast conjugate eye movements that shift gaze between visual targets. They are generated by excitatory burst neurons in the brainstem, which receive input from the cortical eye fields via the superior colliculus. Between saccades, excitatory burst neurons are held off by omnipause neurons (OPN). Inhibitory burst neurons (IBN) inhibit the motoneurons of antagonist muscles during saccades. At the end of the saccade, omnipause neurons resume firing. The cerebellar dorsal vermis and caudal fastigial nucleus are also involved in saccadic accuracy and termination. Given the specific roles that these various neuronal populations play in saccade control, the dysfunction of saccades in neurological disease states can be classified and localized based on the characteristics of the dysfunction. A schematic of five S’s is presented that provides a mechanism to organize saccadic disorders. The S’s include (1) slow saccades, typically due to excitatory burst neuron dysfunction; (2) sticky saccades of ocular apraxia due to cortical eye field lesions; (3) sloppy saccades due to cerebellar hypometria or hypermetria; (4) stunted saccades due to premature firing of the structures involved in saccade termination; and (5) spontaneous saccades that intrude upon fixation due to delayed reactivation of omnipause neurons that unleash the predisposition of burst neurons to oscillate.