Psychopathology and Hepatic Encephalopathy

Authors

  • João Gama Marques Hospital de Júlio de Matos, Centro Hospitalar Psiquiátrico de Lisboa; Faculdade de Medicina da Universidade de Lisboa
  • Diogo Telles-Correia Serviço de Psiquiatria do Hospital de Santa Maria, Centro Hospitalar Lisboa Norte; Faculdade de Medicina da Universidade de Lisboa
  • Manuela Canhoto Serviço de Gastroenterologia; Hospital de Santo André, Leiria

DOI:

https://doi.org/10.25752/psi.3288

Keywords:

Hepatic Encephalopathy, Minimal Hepatic Encephalopathy, Portosys- temic Encephalopathy, Psychopathology, Psychiatry, Liver,

Abstract

Since Hippocrates that neuropsychiatric illness secondary to liver disease fascinates physicians, but only in the XIX century Marcel Nencki and Ivan Pavlov suggested the relation between high concentrations of ammonia and Hepatic Encephalopathy (HE). The reaction of ammonia and glutamate (origins glutamine, “the Trojan Horse of neurotoxicity of ammonia) continues to be the main responsible for the neurologic lesions, recently confirmed by neurochemistry and neuroimagiology studies. Glutamine starts the inflammatory reaction at the central nervous sys- tem but other important actors seem to be manganese and the neurotransmitters systems of GABA and endocanabinoids. Nowadays there are three different etiologic big groups for HE: type A associated with acute liver failure; type B associated with portosystemic bypass; and type C associated with cirrhosis of the liver. The staging of HE is still based on classic West Haven system, but a latent Grade 0 was introduced (the so called minimal HE); remaining the aggra- vating HE from Grade 1 (subtle changes at clinical examination) to Grade 4 (coma). In this work a bibliographic review was made on 30 of the most pertinent and recent papers, focusing in psychopathology, physiopathology, etiology and staging of this clinical entity transversal to Psychiatry and Gastroenterology. Alterations are described in vigility and conscience like temporal, spatial and personal disorientation. Attention, concentration and memory are impaired very early, on latent phase and can be accessed through neuropsychological tests. Mood oscillates between euphoric and depressive. Personality changes begin obviously and abruptly or in a subtle and insidious way. There can be changes in perception like visual hallucinations or even of acoustic-verbal. The thought disorders can be of delusional type, paranoid, systematized or not, but also monothematic ala Capgras Syndrome. Speech can be accelerated, slowed down or completely in- comprehensible. Insight is diminished at the very beginning at minimal HE, especially regarding the car driving abilities. Instinctive life can be impaired as various sleep disorders are present among half of HE patients; loss of appetite is common but there is a case of pica secondary to HE; and libido can seem increased by some pre-frontal type of disinhibition.

Published

2011-08-01

Issue

Section

Review Articles