Micro- and macrovascular changes as the direct cause of parenchymal destruction in congenital murine hydrocephalus.
Microangiotomography was used to identify the normal and pathological pattern of cerebral vessels in the hy-3 murine mutant mouse (normal and hydrocephalic) at various developmental stages from birth through 21 days of life. The technique employed allows resolution, in the range of 7 to 10 mu of the surface and intraparenchymal (perforating) microvasculature. Ventricular enlargement causes displacement of primary cerebral arteries, followed by both stretching and a decrease in the caliber of primary, secondary, and tertiary vessels (arterial and venous). Ultimately, there is a reduction in the number and caliber of the microvasculature, resulting in diminished cerebral blood flow and cerebral edema. Tissue destruction leading to ependymal rupture, parenchymal cavitation, and the formation of porencephalic cysts within the edematous parenchyma ensues. External ventricular drainage, by decompressing the ventricles, resulted in rapid restoration of the filling of the primary and secondary vessels, thereby suggesting the primary role of vascular changes in the production of brain damage. This study offers experimental evidence that early diversion of the cerebrospinal fluid interrupts this chain of events in congenital murine hydrocephalus.
D000818:Animals; D001921:Brain / Q000473:pathology*; D001929:Brain Edema / Q000209:etiology / Q000473:pathology; D002533:Cerebral Angiography; D002536:Cerebral Arteries / Q000473:pathology*; D002552:Cerebral Ventricles / Q000473:pathology; D003287:Contrast Media; D004108:Dilatation, Pathologic; D005110:Extracellular Space; D006849:Hydrocephalus / Q000150:complications / Q000151:congenital / Q000473:pathology*; D051379:Mice; D008815:Mice, Inbred Strains; D008833:Microcirculation / Q000473:pathology*; D014680:Veins / Q000473:pathology
D003287:Contrast Media