| Hauptseite > Publikationsdatenbank > Cerebral water content mapping in cirrhosis patients with and without manifest HE > print |
| 001 | 866641 | ||
| 005 | 20210130003550.0 | ||
| 024 | 7 | _ | |a 10.1007/s11011-019-00427-y |2 doi |
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| 037 | _ | _ | |a FZJ-2019-05720 |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Winterdahl, Michael |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a Cerebral water content mapping in cirrhosis patients with and without manifest HE |
| 260 | _ | _ | |a Dordrecht [u.a.] |c 2019 |b Springer Science + Business Media B.V |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a 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. |
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| 700 | 1 | _ | |a Abbas, Zaheer |0 P:(DE-Juel1)140186 |b 1 |
| 700 | 1 | _ | |a Noer, Ove |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Thomsen, Karen Louise |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Gras, Vincent |0 P:(DE-Juel1)131765 |b 4 |
| 700 | 1 | _ | |a Nahimi, Adjmal |0 P:(DE-HGF)0 |b 5 |
| 700 | 1 | _ | |a Vilstrup, Hendrik |0 P:(DE-HGF)0 |b 6 |
| 700 | 1 | _ | |a Shah, Nadim Joni |0 P:(DE-Juel1)131794 |b 7 |
| 700 | 1 | _ | |a Dam, Gitte |0 0000-0003-3526-0171 |b 8 |e Corresponding author |
| 773 | _ | _ | |a 10.1007/s11011-019-00427-y |g Vol. 34, no. 4, p. 1071 - 1076 |0 PERI:(DE-600)2018067-6 |n 4 |p 1071 - 1076 |t Metabolic brain disease |v 34 |y 2019 |x 1573-7365 |
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