Background: According to the interhemispheric inhibition model of neglect, the uninjured hemisphere inhibits (via the corpus callosum) the injured hemisphere but the injured hemisphere can no longer inhibit the opposite hemisphere, which becomes hyperactive and produces an ipsilesional attentional bias. Alternatively, according to the compensation hypothesis, the uninjured hemisphere helps compensate for the damaged hemisphere, which is impaired in directing attention to contralateral stimuli. If the inhibition model of neglect is correct, callosal disconnection should reduce neglect. If the compensation model is correct, however, it may increase or induce neglect. Patient: A 32-year-old woman, at age 14 years, developed a right frontal astrocytoma and was treated with surgery and radiation but had a cardiopulmonary arrest secondary to aspiration. Subsequent imaging studies revealed damage to the frontal, parietal, and occipital regions of the right hemisphere and damage to the temporal region of the left hemisphere. After discharge, she was able to return to school and drive a car, without any evidence of neglect. About 10 years later, she developed complex partial and atonic seizures that were multifocal and medically intractable. She underwent a complete section of her corpus callosum at age 31 years. Results: One year after the callosal section, she demonstrated (1) diminished spontaneous saccades to the left, hypometric leftward saccades, and left gaze impersistence; (2) left arm hemispatial limb akinesia; (3) unilateral spatial neglect; and (4) motor and cognitive impersistence. Conclusion: In patients with right hemisphere injury, callosal section may induce or enhance motor-intentional deficits and hemispatial neglect.