Mild traumatic brain injury (mTBI) often results in working memory (WM) impairment, but the mechanistic relationship between the two remains elusive. We used a computational model of two cortical neuronal networks linked by myelinated callosal axons with distance-dependent conduction delays to simulate callosal dysfunction in mTBI and quantify its impact on WM. WM maintenance and termination in the model network depended on short-term synaptic plasticity. In injured networks, WM duration depended on the extent of callosal injury, consistent with clinical data. The model provides a framework for studying callosal injury-induced neurobehavioral alterations following mTBI, and, to the best of our knowledge, is the first computational model to address mTBI-induced WM impairment.