Germinal matrix haemorrhage: destroying the brain's building blocks.

Inhibition of Fas-mediated apoptosis through administration of soluble Fas receptor improves functional outcome and reduces posttraumatic axonal degeneration after acute spinal cord injury. ProNGF induces p75-mediated death of oligodendrocytes following spinal cord injury. and delayed degeneration after spinal cord injury in rats and monkeys. Neutralization of CD95 ligand promotes regeneration and functional recovery after spinal cord injury. Nat Med 2004; 10: 389–95. Donnelly DJ, Popovich PG. Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury. A review of the pathophysiology of cervical spon-dylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury. et al. Cell death after spinal cord injury Is exacerbated by rapid TNF alpha-induced trafficking of GluR2-Lacking AMPARs to the plasma membrane. Saenz AD, et al. The cellular inflammatory response in human spinal cords after injury. et al. Tumor necrosis factor-alpha and its receptors contribute to apop-tosis of oligodendrocytes in the spinal cord of spinal hyperostotic mouse (twy/twy) sustaining chronic mechanical compression. Popovich PG. Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. Laudenklos S, et al. CD95-Ligand on peripheral myeloid cells activates Syk kinase to trigger their recruitment to the inflammatory site. Developmental stage of oligodendrocytes determines their response to activated microglia in vitro. et al. Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury. Human neuropathological and animal model evidence supporting a role for Fas-mediated apoptosis and inflammation in cervical spondylotic myelopathy. The most skilled stonemasons cannot construct a cathedral without an ample supply of fine granite blocks. Likewise, the human brain cannot be built properly if stocks of neuroglial progenitors (the building blocks of the brain) are depleted by injury during the critical period of progenitor cell proliferation and migration, as occurs in germinal matrix haemorrhage in prematurity. The article by Prof. Marc Del Bigio (2011), representing the analysis of a career-spanning autopsy cohort of preterm infants with and without germinal matrix haemorrhage, he addresses a persistent clinical concern facing paediatric specialists caring for survivors of prematurity: what are the consequences of germinal matrix haemorrhage on normal brain development at the micro-anatomic level, and do they explain observed neurodevelopmental and neuroimaging outcome data? As a serious complication of prematurity, germinal matrix haemorrhage and its frequent accompaniment, intraventricular haemorrhage , have been recognized in the medical literature …