mice exhibited decreased reactive astrocytosis and increased vascular density, which were reflected by a significant reduction in glial fibrillary acidic protein-expressing-cell area nearest to the ischemic region and an increase in platelet endothelial cell adhesion molecule-1 expression within 1.050 mm adjacent to the lesion border, respectively. Finally, Western blot examinations showed no difference in glial-derived neurotrophic factor and vascular endothelial growth factor expression between the vehicle-and memantine-treated mice; however, there was a significant increase in brain-derived neurotrophic factor and phospho-tyrosine kinase receptor expression near the infarct in memantinetreated mice, suggesting a possible function in peri-infarct recovery and plasticity.We commend López-Valdés et al on their work. The potential for memantine to improve functional outcome in neurological diseases associated with ischemic complications is intriguing. Many diseases seen by neurosurgeons have ischemia as part of their pathophysiology, including, but not limited to, subarachnoid hemorrhage, intracerebral hemorrhage, and embolic stroke from carotid stenosis. Additionally, ischemic injury is a potential complication related to neurosurgical interventions. For this reason, it is our hope that this study will stimulate the conduction of high-quality clinical trials to examine the role of memantine for these difficult clinical problems.