engleski

VULNERABILITY OF THE CORTICAL PATHWAYS IN PERIVENTRICULAR LEUKOMALACIA

In this paper we analyze neuroanatomical substrate of heterogeneous motor, sensory and cognitive deficit caused by periventricular leukomalacia (PVL). The focus of the study was on radial arrangement (from ventricle to pia) fiber-rich compartments, crossroads and axonal strata which determines topography (where?) and cellular targets (what?) for vulnerability of cortical connectivity. The most important temporal factor (when?) is developmental window of intensive growth. Histological sections stained with histochemical and immuno-cytochemical fibrilar markers were compared with diffusion tensor images (DTI) on postmortem fixed brains of human fetuses ranging between 10, 5-28 post-conceptual weeks (PCW) Periventricular pathways (PVP) appear during early fetal life, situated medial to the internal capsule. They form medial component of the periventricular crossroads of pathways. Lateral component of “crossroad” is composed of fibers emerging from internal capsule and developing associative bundles. The medial component of the periventricular crossroads consists of: fronto-occipital bundle, callosal fiber system and cortico-caudate bundle, which run in close proximity to the proliferative cell compartments. Transient components of the periventricular system are fronto-pontine fibers The periventricular fiber system shows intensive growth during mid-gestation from 15-24 PCW, when axons require guidance molecules, extracellular matrix (ECM) substrate. Lateral component of periventricular crossroads consists of projection fibers and deep associative bundles. External to the periventricular crossroads fibers are arranged in sagital strata ; internal, intermediate and external, containing thalamocortical and long associative cortico-cortical pathways. The most external fibers system lies outside external capsule, forming a fibrilar network, and corresponds to the subplate (SP) zone. This prominent zone (SP) contains synaptically driven well differentiated neurons vulnerable to hypoxia, cells producing axonal guidance molecules and ECM substrate. Long cortico-cortical pathways form at the interface between fetal “white” matter and SP. In conclusion, anatomical data suggests different sources and arrangements of periventricular fiber systems, ECM and guidance molecules and one can expect different vulnerability along the radial axis. The most heterogeneous deficit (motor and cognitive) is caused by focal, non-cystic lesion of the medial component of periventricular crossroads. We propose that these pathways also participate in proliferation and migration, which will contribute to the complexity of the lesion. Lesions of the lateral component of the periventricular crossroads will cause sensory and motor deficit. Lesions of sagital strata will show substrate on sensory and cognitive deficit, while the lesions of subplate neurons shows predominantly cognitive deficit. During the growth, afferent and efferent pathways show vigorous structural plasticity. The data presented show early development of vulnerable periventricular pathways and support concept of radial (selective?) vulnerability of embryonic zones and axonal strata. (Supported by Unity through Knowledge Fund project 06/07)

subplate zone

nije evidentirano