Table 3.
Summary of the Main Results Published to Date Using In Vivo MRI/MRS Techniques in Chronic HE Patients.
| HE type | Subjects (n) | Magnetic Field (B0) | Method | Brain region | Type of measurement | Findings |
Comments | Ref | ||
|---|---|---|---|---|---|---|---|---|---|---|
| Edema measurement | Type of edema Cell type | Other | ||||||||
| Liver cirrhosis of different origins HE I+HE II =overt HE |
13-HE-0 12-MHE 10-HE I 3-HE II |
1.5T | Fast absolute measurement of cerebral water content, TAPIR – T1 measure QUTE – quantitative T2∗ image Psychometric testing |
Pu, CR, OWM, FWM, OC, FC, Tha, GP, CN, AL, PL |
In vivo - Single point |
Direct, absolute assessment of water content (%) | N/A |
-↑0.4% water in HE-0, ↑0.8% in MHE, ↑2.1% in overt HE – WM (FWM, OWM) -No significant water content changes in GM, however 1.9%↑ in GP for overt HE |
Correlation between CFF and WM water content | 34 |
| Mild chronic HE Controls |
3 7 |
1.5T | 1H MRS, STEAM, TE=30ms, quantification of 5 metabolites using the scanner data analysis package and ratios to tCr | Midparietal cortex, WM+GM, 12.5-27cm3 |
In vivo - Single point |
N/A | N/A | -trend of ↑Gln and ↓Cho and Ins |
-no statistics due to small number of patients | 136 |
| Liver cirrhosis of different origins Controls |
5-no HE 10-mHE 11-overt HE 14 |
1.5T | T1 weighted images 2D CSI, TE=130ms quantification of 3 metabolites using ratios to Cr Psychometric and EEG testing |
BG, temporal and occipital cortex |
In vivo - Single point |
N/A | N/A | - ↑Glx/Cr and ↓tCho/Cr in patients - no change in NAA/Cr - stronger ↑Glx/Cr in BG - stronger ↓tCho/Cr in occipital cortex |
- patients with no HE – normal spectra - patients with overt HE – abnormal spectra |
137 |
| Liver cirrhosis of different origins |
4-no HE 7-mHE 15-overt HE |
1T | T1 weighted SE images T1 weighted MT images |
BG |
In vivo - Single point |
N/A | N/A | Hyperintensity of GP in 17 patients, and a difference between noHE vs mHE vs overt HE Hyperintensity of Pu in 5 patients |
Relationship between T1 contrast in GP and blood ammonia | 138 |
| Liver cirrhosis of different origins Controls |
24-no HE 4-mHE 4-HE I 6-HE II 1-HE IV 20 |
2T | Routine T1 and T2 weighted images 1H MRS, PRESS, TE=30ms, quantification of 4 metabolites using a Marquardt curve-fitting algorithm and ratios to Cr Neuropsychological tests |
PWM, OGM (2.5cm)3 |
In vivo - Single point |
Indirect indication based on ↓mIns/Cr and ↑Gln/Cr | assumption -Astrocytes swelling |
Asymptomatic (no HE) patients GM: -↓mIns/Cr Subclinical (mHE), overt HE(HE I-IV) GM: -↓mIns/Cr, ↑Gln/Cr -↑NAA/Cr only in over HE Asymptomatic and subclinical HE WM: -↓mIns/Cr Overt HE (HE I-IV) WM: -↓mIns/Cr, ↑Gln/Cr, ↓tCho/Cr |
Correlation between Gln in GM and plasma ammonium (r=0.62) No MRS differences between no HE and mHE MRS differences between mHE and overt HE ↑Gln and ↓mIns with HE grade |
139 |
| Liver cirrhosis of different origins Controls |
8-HE 0 7-HE I 2-HE II 13 |
1.5T |
1H MRS, STEAM, TE=30ms, quantification of 4 metabolites using peak integration and ratios to Cr Neuropsychological tests |
PWM, 18ml | In vivo and longitudinal: 30-60 days after LT or 2weeks after a low protein diet | N/A |
N/A |
-↓mIns/Cr and tCho/Cr in HE - no change in Glx/Cr - no MRS changes observed with diet - no MRS changes 30-60 days after LT |
Correlations: mins/Cr and ammonia with the neuropsychological data | 140 |
| Liver cirrhosis of different origins | 6-mHE 3-overt HE |
1T | Coregistered 3D T1 weighted images Semiautomated contour and thresholding program Neuropsychological tests, EEG |
whole brain and ventricles | In vivo , longitudinal: 6weeks after lactulose (n=7), before and 24h after TIPSS | Indirect indication of low-grade brain swelling | N/A |
No structural abnormalities on T1 weighted images Change in brain and ventricular size after treatment: ↓brain, ↑ventricles and improved psychometric testing (n=3); ↑brain, ↓ventricles and worsen psychometric testing (n=2) |
Blood ammonia (66-98 μmol/L - mHE; 85-130 μmol/L- overt HE) No correlations between MRI, HE and liver function |
88 |
| Liver cirrhosis of different origins Controls MHE |
24-MHE 5-no HE 5-HE I 5-HE II 18 10 |
1.5T | DTI, single shot EPI dual SE sequence, b-value of 1000 s/mm2, 10 directions, MD and FA measured Neuropsychological tests |
CC, RIC, LIC, CN, Pu, FWM, OWM |
In vivo Longitudinal: 3weeks after lactulose in 10 MHE and 10 controls |
Indirect indication ↑MD suggestive of ↑interstitial brain water |
Assumption | No HE - ↑MD in CN MHE - ↑MD in CC, RIC, LIC, CN HE - ↑MD in CC, RIC, LIC, CN, Pu, FWM, OWM -no changes in FA - ↓MD in MHE after lactulose treatment and no change in FA |
MD ↑ from no HE to gr 2 HE- suggestive of increased water with HE grades Correlations between NP and MD in CC, RIC. Correlations between NP and MD in CC. Extracellular migration of macromolecules during the cellular osmoregulatory response may result in ↑ acculmulation of extracellular fluid |
29 |
| Viral liver cirrhosis Controls |
7 –no HE 6-HE I 1-HE II 12 |
1.5T | DWI, b-values:0, 300, 600,900 s/mm2 | CN, Pu, GP, OWM, FWM, PWM, Tha |
In vivo - Single point |
Indirect indication of cytotoxic brain edema | Assumption |
↑ADC in all brain regions except Tha Patient with HE II showed the highest ADC values No differences in ADC between no-HE and HE I Ammonia and related Gln accumulation might contribute to changes in water motility and content |
Correlation between venous ammonia and ADC values in deep gray and WM regions, except CN An increase in cell volume reduces the influence of restriction effects on intracellular diffusion pathways leading to ↑ADC |
64 |
| Liver cirrhosis of different origins | 9-HE 0 6-mHE 6-HE I |
1.5T | T1 weighted images 1H MRS, STEAM, TE=18ms, quantification of 5 metabolites using peak integration and ratios to Cr 13N –ammonia and FDG PET Psychometric examination |
BG, PWM, FGM, 8cm3 |
In vivo - Single point |
N/A | N/A | MRS changes significant if patients divided into Child classes but not in HE classes -↓mIns/Cr in all 3 brain regions from Child A to C -↓tCho/Cr in BG, GM from Child A to C -↑Glx/Cr in BG, WM from Child A to C -↑NAA/Cr in WM from Child A to C |
No controls Correlations: -psychometric HE score with Glx/Cr in BG -venous plasma ammonia with MRS in WM -cerebral glucose utilization with mIns/Cr |
141 |
| Liver cirrhosis of different origins |
27 |
1.5T | T2 weighted, FSE Fast FLAIR images Neurologic assessment |
WM |
In vivo, longitudinal: before and after LT | Indirect indication of brain edema | N/A | -focal lesions were identified on the T2 weighted images before LT compatible with small-vessel brain disease in 19 patients - after LT (6-14 months)– average of 21.7% decrease of Wm lesion volumes |
No association between WM lesion, age, cause of cirrhosis, Child-Pugh score or laboratory findings Correlation: WM lesions and percent improvement in overall cognitive function |
90 |
| Cirrhotic patients with HE | 3 | No detail | FLAIR images | WM | In vivo, longitudinal | Indirect indication of brain edema | N/A | -supratentorial focal and diffuse WM lesions compatible with small-vessel brain disease which reduced with improvement of HE | - these changes were associated with brain edema and support the participation of BBB in the pathogenesis of brain edema in HE | 89 |
| Liver cirrhosis of different origins Controls |
20-no HE 10-mHE 24 |
1.5T | DWI, single shot EPI sequence Neuropsychological tests |
Pu, GP, Tha, posterior cingulate GM, FWM, PWM |
In vivo - Single point |
Indirect indication of minimal cellular edema | -↑ ADC in mHE in WM compared to no HE -no difference in noHE compared to controls for ADC values |
Correlations: ADC in WM with venous ammonia; ADC in WM and neuropsychological tests minimal cellular edema with an increase of membrane permeability and increased intracellular diffusivity, as well as changes in the viscosity of the cytoplasm |
65 | |
| Liver cirrhosis of different origins Controls |
33-mHE 30 |
1.5T | Proton density, T2 weighted images T1 weighted images, MPRAGE sequence 1H MRS, 2D L-COS, TE=30ms, quantification of 13 metabolites using Felix NMR software and ratios to Cr Neuropsychological tests |
GP Occipital and prefrontal lobe, 27cm3 |
In vivo - Single point |
N/A | N/A | -↑GP signal intensity -↑Glx/Cr in both brain regions -↓mICh/Cr, mIns/Cr and Ch_d/Cr in both brain regions |
Correlations between NP tests and MRS ratios mICh – most discriminant variable |
142 |
| Liver cirrhosis and overt HE Controls |
41 16 |
1.5T | T2 weighted, FSE T1 weighted, SE DTI, single shot EPI sequence, 6 noncollinear directions, 11b-values (0-7500s/mm2), mono and bi-exponential fitting Neuropsychological tests |
PWM, corticospinal tract |
In vivo, longitudinal: before and 1 year after LT (n=24) | Indirect indication of increased brain water content based on ↑MD | assumption interstitial edema |
-↑MD for fast diffusion in PWM which returned to normal after LT -↓FA that increased after LT -↑MD for fast and slow diffusion in corticospinal tract, only fast MD returned to normal after LT -↓ fast FA in corticospinal tract with a persistent decrease after LT |
- edema is reversible after LT but some microstructural changes might persist along the corticospinal tract as suggested by evolution of FA - extracellular edema - PWM - mixed edema -corticospinal tract No association between DTI parameters and neuropsychological tests |
22 |
| Viral cirrhosis Controls |
28 28 |
3T | 3D FLAIR sequence Brain volume, vertex based shape analysis – FIRST/FSL software Total intracranial volume – Gaser’s VBM5 toolbox with SPM5 Neuropsychological tests |
DGM (NC, Amy, CN, Hip, GP, Pu, Tha) |
In vivo, single point | N/A | N/A |
↓ volume in CN and Pu - a smaller volume was proportional to the severity of the disease -shape alteration in Pu, CN and GP |
Correlations: decreased DGM volume with poorer cognitive results | 47 |
| Multiparametric studies / Multimodal studies | ||||||||||
| Non-alcoholic cirrhosis Controls |
24 (16 with mHE) 8 |
1.5T | T2 weighted, FSE T1 weighted, IR SE MT, 2D GE 1H MRS, STEAM, TE=20ms, quantification of 5 metabolites using AMARES and ratios to tCr Neuropsychological tests |
PWM; FWM Parietal WM, 8cm3 |
In vivo, single point | Indirect indication of low grade intracellular swelling (↑ water content) based on ↓MTR | assumption |
No changes in T2 weighted images ↑T1 signal intensity in BG and GP index ↓MTR in PWM and FWM ↑Glx/Cr in mHE only in PWM ↓mIns/Cr and Cho/Cr in all patients in PWM No changes in NAA/Cr |
Correlations: MTR with Glx/Cr; MTR with GP index | 56 |
| Nalc cirrhosis without overt HE (70% mHE) After LT Controls |
24 11 10 |
1.5T | T2 weighted, FSE T1 weighted, IR SE MT, 2D GE 1H MRS, STEAM, TE=20ms, quantification of 5 metabolites using AMARES and ratios to Cr Neuropsychological tests |
PWM; FWM Parieto-occipital WM, 8cm3 |
In vivo Longitudinal: before and after LT at 1 month and 1 year |
Indirect indication of low grade edema (↑ water content) based on ↓MTR | N/A | No changes in T2 weighted images ↑T1 signal intensity in BG ↓MTR in PWM and FWM ↑Glx/Cr in mHE only ↓mIns/Cr and Cho/Cr in all patients No changes in NAA/Cr After LT: improvement in MTR; normalization of 1H MRS findings with a lower normalization for mIns/Cr; slower normalization of T1 hyperintensity in GP; neuropsychological impairment showed a rapid improvement |
Correlations between MTR and Glx/Cr and plasma osmolarity Glx/Cr and mIns/Cr correlated with liver and neuropsychological function No correlation between MTR and neuropsychological function Low grade edema and mHE are associated with ↑Gln –manifestations of metabolism of ammonia |
57 |
| PBC stage I-II PBS stage III-IV Controls |
14 4 11 |
1.5T | SE proton density image MT 1H MRS, PRESS, TE=135ms, quantification of 3 metabolites using the scanner software (Philips) |
GP, CN, Pu, Tha, FWM 8cm3, in BG and WM |
In vivo - Single point |
N/A | N/A |
↓MTR in GP No changes in 1H MRS |
Correlations between MTR and fatigue and MTR and blood manganese MTR changes are not a consequence of HE but rather of altered manganese homeostasis |
143 |
| Liver cirrhosis Alcoholics Nonalcoholics Controls |
26 16 18 |
1.5T |
1H MRS, STEAM, TE=20ms, 5 metabolites quantified using LCModel and ratios to Cr MT, 2D GE images DWI, single shot SE EPI, b-values: 0-500-1000 s/mm2, 3 directions Neuropsychologic examination |
Left OWM and BG, 8cm3 Tha, pons, OWM, GP, Pu, CN Tha, pons, OWM |
In vivo-single point | Indirect indication of ↑water content based on ↓MTR | N/A |
Nalc group in BG: ↓mIns/Cr, Cho/Cr and ↑Glx/Cr Nalc group in OWM: ↓mIns/Cr and ↑Glx/Cr, NAA/Cr Alc group in BG: ↓mIns/Cr, Cho/Cr and ↑Glx/Cr Alc group in OWM: ↓mIns/Cr and ↑Glx/Cr MRS changes were significant for overt HE and similar in GM and WM ↓ MTR in both groups No change in ADC only a small trend of ↑ with increasing HE |
Correlations in Nalc: mIns/Cr and Glx/Cr with HE in both regions and MTR with HE Other correlations are presented No correlations in Alc group MR differences between Alc and Nalc –possible microstructural lesions due to chronic alcohol abuse |
144 |
| Liver cirrhosis of different causes and overt HE Liver cirrhosis without overt HE Controls |
24-overt HE 9 9 |
1.5T | DWI, b-values: 0-500-1000 s/mm2 MT, 3D GE images 1H MRS, TE=31ms, no sequence mentioned, 5 metabolites quantified using AMARES and ratios to Cr |
GP, Pu, Tha, Hip, CR, PGM, PWM 2x2x2cm3, PWM |
In vivo Longitudinal:24h after diagnosis and 5 days after resolution of HE episode | Indirect indication of ↑water content/low grade edema based on ↓MTR and ↑Glx/Cr, ↓Ins/Cr | assumption |
-No change in mean ADC between HE and non-HE patients ↓MTR in non-HE ↓↓MTR in HE in GP and PGM Glx/Cr –median =1.8 controls, 2.4 non-HE and 4.4 in HE. Ins/Cr – similar between HE and non-HE but lower than controls 5 days after no change in MTR, Glx/Cr, Ins/Cr but a ↓ADC in PGM |
Correlation between MTR and Glx/Cr in WM in HE patients ↓ADC 5 days after – water flux from extracellular to intracellular compartment Brain regional difference – WM stronger water increase Small number of patients |
145 |
| Liver cirrhosis no evidence of overt HE | 24 |
1.5T | Proton density and T2 weighted FSE T1 weighted SE imaging - Brain volume – SIENAX from FSL 1H MRS, PRESS, TE=30ms, metabolites quantified using LCModel and ratios to Cr Neuropsychological assessment (n=52) |
Parieto-occipital WM, 8cm3 |
In vivo, single point: 6 to 12 months post LT | N/A | N/A |
Improvement in neuropsychological tests after LT except for 7 patients Brain smaller volume showed poorer function on motor tests Bain metabolites were in normal range |
MRI and MRS data only after LT HE has an effect on cognitive function after LT, likely because it results in neuronal and brain volume loss |
53 |
| Stable liver cirrhosis of different causes (no-HE+mHE) |
13 | 3T | 3D T1 weighted, T2 weighted and FLAIR DTI, EPI, 2 b values:0-1000s/mm2, 6 directions 1H MRS, PRESS, TE=36ms, 6 metabolites quantified using QUEST/jMRUI and water as internal reference Psychometric tests: PHES, CDRS |
WM Frontal WM, 8cm3 |
In vivo Longitudinal at 0, 140 and 170 min after ingestion of amino acid capsules |
Indirect indication of in changes in brain water compartmentalization based on ↑trADC | N/A |
No change in the CDRS after challenge ↑trADC (9%) after the challenge ↓Ins after challenge, no change in Gln, Glu, NAA, Cr, Cho No change in brain volume. Ammonia can directly drive changes in water distribution. No vasogenic mechanisms146 |
No controls Correlations: changes in trADC vs blood ammonia, changes in blood ammonia vs brain Gln, changes in trADC and brain Ins Glial swelling and redistribution of extra-intracellular water during HA – likely mechanisms of edema in HE146 |
51 |
| Liver cirrhosis of different causes Controls |
6-HE II 10-HE III 2-HE IV 8 |
3T | Proton density and T2 weighted FSE and fast FLAIR T1 weighted imaging DWI, single shot EPI, 4 b values:0-3000s/mm2 1H MRS, PRESS, TE=30ms, 5 metabolites quantified using LCModel and ratios to Cr HE patients: lactulose and rifaximin-severity grades were lower for the MRI |
PWM, corticospinal tract WM-parieto-occipital region, 8cm3 |
In vivo –first 5 days after hospitalization Longitudinal – 6 weeks later (n=14) |
Indirect indication of extracellular edema based on ↑ADC which returned to normal after 6 weeks | assumption |
↑ADC in patients vs controls ↑Gln/Cr in HE patients vs controls (2.4±0.78 vs 0.22±0.08) ↓Ins/Cr and Cho/Cr No change for Glu/Cr and NAA/Cr ↓ADC, ↓Gln/Cr and ↑Ins/Cr after 6 weeks in patients recovering after HE ADC in PWM similar to controls but ↑ in corticospinal tract 6 weeks after |
Correlations: Gln/Cr with HE grades, Gln/Cr and blood ammonia ↑ADC in patients with dehydration, ↓Ins/Cr in patients with hyponatremia Brain edema does not seem to be directly responsible for the neurological manifestation |
23 |
| Well-compensated liver cirrhosis of different causes and previous mHE Controls |
22 21 |
3T | Volumetric imaging – 3D T1weighted sequence, SIENA – FSL software FSL fMRI, visuomotor task 1H MRS, PRESS, TE=36ms, 4 metabolites quantified using ratios to Cr Psychometric testing: CDRS, PHES |
8cm3, left BG |
In vivo Longitudinal: 4weeks after LOLA |
N/A | N/A |
No change in brain volume No change in activation after visual task before and after LOLA Greater activation in motor task after LOLA No Change in Glx/Cr, Cho/Cr, Ins/Cr, NAA/Cr pre and post-LOLA |
Improvements in CDRS and PHES after LOLA Correlations between the fMRI and psychometric tests |
52 |
| Liver cirrhosis with mHE | 20 | 3T | DTI, single shot SE EPI, b=1000s/mm2, 60 directions, FA, MD –FSL tool 1H MRS, PROBE, TE=35ms, 4 metabolites quantified using LCModel and ratios to Cr fMRI, 2 tasks: N-back and inhibitory control tests Cognitive testing |
12 ROI – e.g. FWM, pWM, CC, IC, EC, cingulum ACC; pGM, rpWM, 8cm3 |
In vivo Longitudinal: before and 8 weeks after rifaximin treatment |
N/A |
↑FA, no change in MD, imply cytotoxic edema correction |
No changes in MD Small ↑FA in 5 ROIs after rifaximin No metabolite changes before and after rifaximin Higher activation in some brain areas after rifaximin |
Improvement in cognitive tests after rifaximin Improvement in WM integrity after rifaximin No control or placebo group |
93 |
| Liver cirrhosis with mHE or HE I Controls |
30 16 |
3T |
1H MRS, MEGA-PRESS, TE=68ms, 4 metabolites quantified using LCModel and ratios to Cr Fast absolute measurement of cerebral water content34 Psychometric tests |
Occipital lobe, sensory and motor cortex–“hand knob”, 27cm3 each |
In vivo - single point |
Direct, absolute assessment of water content (%) |
N/A |
↑Gln/Cr in mHE and HE 1 in both voxels ↓Ins/Cr in mHE and HE 1 in both voxels compared to controls ↑GSx/Cr in mHE and HE 1 ↓GABA/Cr in mHE and HE1 in occipital lobe No change in water content MEGA-PRESS sequence was optimized for GABA and not glutathione. |
Correlations: Gln/Cr with blood ammonia and CFF; Ins/Cr with ammonia and CFF, ↑GSx/Cr with ammonia Several other correlations are mentioned Edema is only marginally responsible for symptoms of covert HE |
147 |
| Liver cirrhosis Alc (n=46) Nalc (n=102) No Controls |
19-no HE 27-HE 48-no HE 44-HE |
1.5T Two sites |
T1 weighted images (MPRAGE) -VBM using FSL-VBM DTI, single shot SE EPI, b=1000s/mm2, 30 directions, FA, MD, CS –FSL tool 1H MRS, PRESS, TE=35ms, 4 metabolites quantified using LCModel and ratios to Cr |
13 ROI – e.g. FWM, pWM, CC, IC, cingulum ACC; pGM, rpWM, 8cm3 |
In vivo Longitudinal: 1 year after |
Indirect indication of interstitial edema based on ↑MD and CS | assumption |
GM density reduced in Alc vs Nalc Alc vs Nalc: ↓FA, ↑MD, ↑CS in all ROI HE status affects Nalc (FA and CS) Alc vs Nalc: ↑Glx, ↓Ins (rpWM, ACC), ↓Ins (pGM) no HE: ↑Glx, ↓Ins HE: no difference In Nalc HE: ↑Glx in all 3 regions |
No changes in brain metabolites 1 year later |
148 |
| Liver cirrhosis Controls |
7-no HE 7-mHE 6 |
3T | T2 weighted, FLAIR and T1 weighted images (MPRAGE/SPGR sequence) DWI* MT* Neuropsychological tests Blood ammonia and cytokines |
FWM, PWM, IC, BG |
In vivo Longitudinal: 8 weeks after lactulose and rifaximin treatment | Indirect indication of low-grade brain edema in mHE based on ↓MTR | N/A |
Diffuse atrophy–47.9% of patients Hyperintensity in BG-60.8% of patients No DWI results ↓ MTR in mHE in FWM, PWM, IC and BG compared to controls ↓ MTR in mHE compared to non HE – PWM, IC, BG ↑MTR after treatment except for BG in mHE No change in MTR in no HE after treatment |
Correlations: -IL-6 with MTR in PWM and IC -ammonia with MTR in PWM -NP with MTR in PWM, IC -no correlations after treatment ↑ammonia in mHE and noHE with mHE>no HE ↑IL-1 and IL-6 in mHE |
48 |
| Cirrhotic patients of different causes Controls |
26 19 |
3T | Volumetric imaging – 3D T1weighted sequence, T2 weighted sequence DTI, single-shot EPI sequence, 32 directions, b=1000s/mm2, ADC and FA measured, DTI Studio software MT, 2D GE, ImageJ software Psychometric testing |
Genu, body and splenium of CC, ACR, PCR FWM, Pu, GP, Tha, CN |
In vivo-single point | Indirect indication based on ↓MTR and ↑ADC | Assumption |
No change in total brain volume ↑ADC in genus and body of CC No difference in FA ↓MTR in GP (5.8%), FWM (4%), CN, Pu, 8 patients had mHE |
Trend of ↓MTR in mHE compared with other patients in FWM in GP Trend of ↓MTR in patients with alcohol-related disease ↓MTR and ↑ADC might demonstrate cytoplasmic changes of astrocytes Changes in astrocytes membrane permeability /redistribution of macromolecules |
50 |
| Well-compensated liver cirrhosis of different causes Controls |
22 22 |
3T | Volumetric imaging – 3D T1weighted sequence, FMRIB software (FSL) T2 weighted sequence DTI, single-shot EPI sequence, 15 directions, b=1000s/mm2, ADC and FA measured, DTI Studio software MT, 2D GE, ImageJ software 1H MRS, PRESS, TE=36ms, 5 metabolites quantified using AMARES and ratios to Cr Psychometric testing |
FWM, Pu, GP, Tha, CN Genu, body and splenium of CC 15x15x15mm3, left BG |
In vivo Longitudinal: 4weeks after LOLA |
N/A | N/A |
No change in total brain volume No change in ADC or FA nor in their relation to neuropsychiatric status ↓MTR in GP, Tha in patients with cirrhosis ↓MTR in FWM only in mHE No change in metabolite ratios 7 patients out of 22 had mHE |
Psychometric performance was improved in 4 mHE patients after LOLA. No other changes were found after LOLA |
49 |