Neurosurgical procedures often involve, as a result of the surgeon approaching the diseased region, unavoidable trauma to the adjacent, non-diseased brain structures. Because of the priority of removing the immediate threats to health or life that underlie such interventions, side effects of surgical brain injuries were not given much attention until recently. The cause-and-effect association of the eventual delayed cognitive and/or neurological deficits is often obscure due to substantial potential of the brain for compensatory changes, long life span in man, and aging-related phenomena. However, animal and human studies have demonstrated that physical insults to the brain can initiate a cascade of changes that results, in the long run, in massive neurodegeneration and brain atrophy. Here we present a review of morphological and ultrastructural findings obtained mostly in a rat model of surgical neocortex injury, with consideration of the current view of this region as a network of specific neurovascular units. The neurovascular unit is a dynamic assembly consisting of a capillary vessel, pericytes, neurons and capillary-bound astrocytes. The integrity of this building block and the interactions between its component parts are responsible, among other things, for the proper functioning of the blood-brain barrier, brain blood circulation and the brain as a whole, and its dysregulation is associated with many CNS pathologies. The studies performed in the rat model of surgical brain injury presented in this review have brought new interesting findings regarding the consequences of such damage to the (ultra)structure and hence presumably to the function of the unit. These findings may have some relevance to human clinical situations.