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@ARTICLE{Winterdahl:866641,
author = {Winterdahl, Michael and Abbas, Zaheer and Noer, Ove and
Thomsen, Karen Louise and Gras, Vincent and Nahimi, Adjmal
and Vilstrup, Hendrik and Shah, Nadim Joni and Dam, Gitte},
title = {{C}erebral water content mapping in cirrhosis patients with
and without manifest {HE}},
journal = {Metabolic brain disease},
volume = {34},
number = {4},
issn = {1573-7365},
address = {Dordrecht [u.a.]},
publisher = {Springer Science + Business Media B.V},
reportid = {FZJ-2019-05720},
pages = {1071 - 1076},
year = {2019},
abstract = {Hepatic encephalopathy (HE) is a frequent and debilitating
complication of cirrhosis and its pathogenesis is not
definitively clarified. Recent hypotheses focus on the
possible existence of low-grade cerebral edema due to
accumulation of osmolytes secondary to hyperammonemia. In
the present study we investigated increases in cerebral
water content by a novel magnetic resonance impedance (MRI)
technique in cirrhosis patients with and without clinically
manifest HE. We used a 3 T MRI technique for quantitative
cerebral water content mapping in nine cirrhosis patients
with an episode of overt HE, ten cirrhosis patients who
never suffered from HE, and ten healthy aged-matched
controls. We tested for differences between groups by
statistical non-parametric mapping (SnPM) for a voxel-based
spatial evaluation. The patients with HE had significantly
higher water content in white matter than the cirrhosis
patients $(0.6\%),$ who in turn, had significantly higher
content than the controls $(1.7\%).$ Although the global
gray matter water content did not differ between the groups,
the patients with HE had markedly higher thalamic water
content than patients who never experienced HE $(6.0\%$
higher). We found increased white matter water content in
cirrhosis patients, predominantly in those with manifest HE.
This confirms the presence of increasing degrees of
low-grade edema with exacerbation of pathology. The thalamic
edema in manifest HE may lead to compromised basal
ganglia-thalamo-cortical circuits, in accordance with the
major clinical symptoms of HE. The identification of the
thalamus as particularly inflicted in manifest HE is
potentially relevant to the pathophysiology of HE.},
cin = {INM-4 / INM-11 / JARA-BRAIN},
ddc = {610},
cid = {I:(DE-Juel1)INM-4-20090406 / I:(DE-Juel1)INM-11-20170113 /
$I:(DE-82)080010_20140620$},
pnm = {573 - Neuroimaging (POF3-573)},
pid = {G:(DE-HGF)POF3-573},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31089866},
UT = {WOS:000475697800012},
doi = {10.1007/s11011-019-00427-y},
url = {https://juser.fz-juelich.de/record/866641},
}