Studies of human amnesia provide evidence for a short-term memory store with information transfer to long term memory occurring within 60 s of sensory encoding. Human and nonhuman primate research has shown that maintenance of this short-term or working memory store is dependent upon frontal cortical activation, although the critical temporal parameters of frontal involvement throughout this 60-s window are undetermined. We examined prefrontal contributions to rapid (under 2 s) and sustained (over 4 s) visual working memory by recording behavioral performance and event-related potentials (ERPs) in patients with lesions in dorsolateral frontal cortex and age-matched control subjects. Prefrontal lesioned patients generated a reduced sustained frontal positivity at all delays. At short delays, patients generated reduced performance to stimuli presented in the contralesional field. Patients generated a negative potential (N400), greatest to contralesionally presented stimuli, that was observed in the control subjects only at long delays. The results indicate that prefrontal lesions impair the frontal component of an anterior-posterior working memory network activated during rapid and sustained visual memory processing. Frontal patients may require activation of limbic cortex, indexed by N400, for maintenance of both rapid and sustained working memory.