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Type:
Educational Exhibit
Keywords:
Metabolic disorders, Cirrhosis, Diagnostic procedure, MR-Spectroscopy, MR-Diffusion/Perfusion, MR, Neuroradiology brain
Authors:
L. Farras Roca1, J. J. Sánchez Fernández2, P. Puyalto3, P. Mora Montoya2, M. Cos Domingo2, C. M. Grassi Zamora2, D. S. Palominos Pose2, J. C. Sardiñas Barrero2, C. Majós Torró2; 1Barcelona/ES, 2L\' Hospitalet de Llobregat-Barcelona/ES, 3Badalona/ES
DOI:
10.1594/ecr2016/C-1352
Background
Hepatic encephalopathy can occur in the setting of acute fulminant hepatic failure or as a more chronic disease,
which is usually a more indolent process.
Although its pathogenesis is not clear and many hypotheses have been proposed,
the physiopatothology is thought to be due to the cerebral edema and raised intracranial pressure caused by an increased intracellular osmolytes,
which are usually metabolized by the liver,
such as manganese and ammonia.
The clinical manifestations are secondary to a misbalance between inhibitory and excitatory neurotransmission.
This misbalance can be consequence of two main factors: a downregulation of glutamate receptors,
secondary to inactivation of the glutamate transporter in astrocytes in liver failure; and an increase in inhibitory neurotransmission due to increased levels of natural benzodiazepines and increased availability of GABA-aminobutyric acid.
In the majority of cases,
there’s a precipitating cause rather than worsening of hepatocellular function can be identified.
Infection is the main leading etiology (50%) in patients with hepatic dysfunction.
Hepatic encephalopathy includes a spectrum of neuropsychiatric abnormalities occurring in patients with liver dysfunction,
ranging from mild deficits in psychomotor abilities to confusion and finally stupor in higher grades.
The neurologic manifestations are mainly due to the shunt of blood arising from the portal venous system to the systemic circulation and are reversible once the liver function abnormality or precipitating factor has been corrected.