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Ventriculomegaly is an increase in cerebral ventricular dimensions. It could be secondary to increased cerebrospinal fluid pressure in the ventricular cavity (hydrocephalus), or to a lack of brain parenchyma due to atrophic involution or arrested development. Ventriculomegaly causes diagnostic, therapeutic, and prognostic dilemma for obstetricians,...
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Context 1
... mild or borderline VM is well defined and got an accepted norms among radiologists, there is no accepted definitions for grading moderate or se- vere VM. Most define them as moderate to severe VM ( Fig. 1). Fetal cerebral VM is defined as an axial diame- ter >10 mm across the atrium of the posterior or anteri- or horn of lateral ventricles at any gestation through TA scans. The atrial diameter is constant at 7.6 ± 0.6 mm (mean ± SD) from 14th to 38th weeks of gestation ...
Context 2
... are also of great value for prognos- tication and obstetric management. Whether VM is isolated or associated with other malformation, non- progressive or progressive will affect the management and prognosis of VM (Figs 1-5). ...
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Citations
... Fetal intracranial hemorrhage (ICH) is a major risk for hydrocephalus (posthemorrhagic hydrocephalus, PHH)[131,142,143]. PHH is a common neurological disorder characterized by increased head size, cortical thinning, ventricular cerebrospinal fluid accumulation, and ventriculomegaly. ...
LPA is a bioactive phospholipid with a plethora of roles in the developing and adult nervous system. LPA signaling mediates many processes in the brain including survival, development and function of neural progenitor cells, astrocytes, oligodendrocytes, and microglia. The intricate spatiotemporal pattern of LPA metabolism and receptor expression are critical for normal CNS development; altered LPA signaling underlies fetal lethality, neurodevelopmental deficits, and is associated with neuropsychiatric impairments and cognitive decline. Fetal hypoxic and hemorrhagic injuries are major causes for neurodevelopmental defects and these injury mechanisms are linked to changes in LPA signaling during critical periods of corticogenesis. This chapter will focus on the role of LPA in neurogenesis of the developing brain and the contribution of aberrant LPA signaling and metabolism in the pathogenesis of neurodevelopmental diseases.
