Developmental Neuropathology and Outcome of Perinatal Brain Damage and the Brain Microvascuar System

The cerebral cortex microvascular system of normal (unaltered) brains is described and compared with that of altered ones by perinatal brain damage. The brain’ microvascular system evolves from the pial capillary plexus an important meningeal compartment poorly studied. A pial capillary anastomotic plexus already cover the cortex in 6-week-old embryos, although its vascularization will not start until the eight-week. This plexus expands covering cortex entire surface throughout life. The cortex has two basic intracerebral microvascular compartments: an extrinsic one represented by the perforating vessels and an intrinsic one represented by the anastomotic capillary plexus established among contiguous perforators. Throughout the developing and the adult cortex, the perforating vessels are separated from each other by a distance raging from 400 to 600 micrometers. The equidistant distance among perforators is considered to represent a biological constant necessary for the functional activity of gray matter neurons. All perforating vessels are within the Virchow-Robin Compartment and hence extrinsic to the nervous tissue. This compartment remains open to the meningeal interstitium and serves as the cortex sole drainage system (mammals’ brain lacks a lymphatic system). The cortex’ intrinsic microvascular compartment is represented by the anastomotic capillary plexus established between contiguous perforators. The neurons, glial cells, fibers terminals and synaptic profiles within the intrinsic microvascular compartment represent the functional center of each cortical region. The interexchange of information among these elements determines the blood flow through each region in response to its neurons functional demands. Each cortical region may function independently or in combination with proximal as well as distant regions functionally interconnected with it. There are more perforating vessels and intrinsic capillaries in the gray than in the white matter, which explains their different neuronal activities and different vulnerabilities to perinatal brain damage. In hemorrhagic and/or ischemic brain lesions, damaged intrinsic capillaries are replaced by post-inflammatory ones, which lack their functional efficiency. In any reappeared cortical lesion, the local neurons, intrinsic neuropil and vascularitywill are transformed. Local neuronal alterations could affect the functional activity of proximal and distant regions interconnected with them and eventually the whole brain. This ongoing mechanism could play a role in the pathogenesis of neurological sequelae secondary to perinatal brain damage.