title: Acute hepatic encephalopathy: diffusion-weighted and fluid-attenuated inversion recovery findings, and correlation with plasma ammonia level and clinical outcome.
abstract: OBJECTIVE
  In acute hepatic encephalopathy, MR imaging abnormalities have been described in the PVWM, thalami, and corticospinal tracts. We sought to determine characteristic regions of involvement on FLAIR and DWI, to evaluate their reversibility, and to correlate MR imaging extent with clinical severity.
  
  
  METHODS
  Twenty patients who presented clinically with acute hepatic encephalopathy and MR imaging <21 days after symptom onset were reviewed retrospectively. Two neuroradiologists recorded involved regions on FLAIR and DWI in each, measured ADC values in affected regions and NAWM, and scored the MR imaging severity/extent. The initial severity (West Haven grade), follow-up clinical severity (degree of improvement), and maximal PAL within ±8 days of MR imaging were recorded and correlated with the MR imaging severity.
  
  
  RESULTS
  On FLAIR and DWI respectively, there were abnormalities in the thalami (85%, 70%), PLIC (75%, 80%), PVWM (80%, 85%), and DBS (70%, 35%) and diffuse cortical involvement (30%, 25%). There were relatively strong significant (P < .005) correlations of FLAIR (r = 0.680, P = .001) and DWI severity (r = 0.690, P = .001) with PAL, and of PAL with the clinical outcome (r = 0.691, P = .001). Both FLAIR (r = 0.592, P = .006) and DWI (r = 0.487, P = .029) severity correlated moderately with the clinical outcome but were not significant at the P < .005 level after Bonferroni correction.
  
  
  CONCLUSIONS
  Patients with acute hepatic encephalopathy may exhibit characteristic regions of involvement on FLAIR with DWI findings that can be reversible. The MR imaging extent on FLAIR and DWI strongly correlates with the maximal PAL, and PAL correlates well with the clinical outcome. Diffuse cortical involvement has a higher potential for neurologic sequelae but can be reversible.
authors.affiliation: Department of Radiology, University of Minnesota, Minneapolis, MN 55455, USA. mckinrad@umn.edu
authors.forename: A M
authors.initials: AM
authors.lastname: McKinney
authors.forename: B D
authors.initials: BD
authors.lastname: Lohman
authors.forename: B
authors.initials: B
authors.lastname: Sarikaya
authors.forename: E
authors.initials: E
authors.lastname: Uhlmann
authors.forename: J
authors.initials: J
authors.lastname: Spanbauer
authors.forename: T
authors.initials: T
authors.lastname: Singewald
authors.forename: J R
authors.initials: JR
authors.lastname: Brace
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000641:Ammonia / Q000097:blood*; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D002648:Child; D038524:Diffusion Magnetic Resonance Imaging; D005260:Female; D005500:Follow-Up Studies; D006501:Hepatic Encephalopathy / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D022124:Hyperammonemia / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D020127:Recovery of Function; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013788:Thalamus / Q000378:metabolism / Q000473:pathology; D055815:Young Adult
chemical_list: D000641:Ammonia
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