@article{10902/37581,
year = {2018},
month = {9},
url = {https://hdl.handle.net/10902/37581},
abstract = {Introduction: Since its description five decades ago, the pathophysiology of idiopathic chronic adult hydrocephalus (iCAH) has been traditionally related to the effect that ventricular dilatation exerts on the structures surrounding the ventricular system. However, altered cerebral blood flow, especially a reduction in the CSF turnover rate, are starting to be considered the main pathophysiological elements of this disease.
Development: Compression of the pyramidal tract, the frontostriatal and frontoreticular circuits, and the paraventricular fibres of the superior longitudinal fasciculus have all been reported in iCAH. At the level of the corpus callosum, gliosis replaces a number of commissural tracts. Cerebral blood flow is also altered, showing a periventricular watershed region limited by the subependymal arteries and the perforating branches of the major arteries of the anterior cerebral circulation. The CSF turnover rate is decreased by 75%, leading to the reduced
clearance of neurotoxins and the interruption of neuroendocrine and paracrine signalling in the CSF.},
publisher = {Elsevier Doyma},
publisher = {Neurologia, 2018, 33(7), 449-458},
title = {Current concepts on the pathophysiology of idiopathic chronic adult hydrocephalus: are we facing another neurodegenerative disease?},
author = {Martín Láez, Rubén and Valle San Román, N. and Rodríguez Rodríguez, Eloy Manuel and Marco de Lucas, Enrique and Berciano, José Ángel and Vázquez Barquero, Alfonso},
}