MR Imaging Findings in Hepatic Encephalopathy

Abstract

SUMMARY:The term hepatic encephalopathy (HE) includes a spectrum of neuropsychiatric abnormalities occurring in patients with liver dysfunction. Most cases are associated with cirrhosis and portal hypertension or portal-systemic shunts, but the condition can also be seen in patients with acute liver failure and, rarely, with portal-systemic bypass and no associated intrinsic hepatocellular disease. Although HE is a clinical condition, several neuroimaging techniques, particularly MR imaging, may eventually be useful for the diagnosis because they can identify and measure the consequences of central nervous system (CNS) increase in substances that under normal circumstances, are efficiently metabolized by the liver. Classic MR imaging abnormalities include high signal intensity in the globus pallidum on T1-weighted images, likely a reflection of increased tissue concentrations of manganese, and an elevated glutamine/glutamate peak coupled with decreased myo-inositol and choline signals on proton MR spectroscopy, representing disturbances in cell-volume homeostasis secondary to brain hyperammonemia. Recent data have shown that white matter abnormalities, also related to increased CNS ammonia concentration, can also be detected with several MR imaging techniques such as magnetization transfer ratio measurements, fast fluid-attenuated inversion recovery sequences, and diffusion-weighted images. All these MR imaging abnormalities, which return to normal with restoration of liver function, probably reflect the presence of mild diffuse brain edema, which seems to play an essential role in the pathogenesis of HE. It is likely that MR imaging will be increasingly used to evaluate the mechanisms involved in the pathogenesis of HE and to assess the effects of therapeutic measures focused on correcting brain edema in these patients. Hepatic encephalopathy (HE) reflects a spectrum of neuropsychiatric abnormalities occurring in patients with liver dysfunction. Most cases are associated with cirrhosis and portal hypertension or portal-systemic shunts, but the condition can also be seen in patients with acute liver failure and, rarely, with portal-systemic bypass and no associated intrinsic hepatocellular disease.1,2 The most common clinical pattern in these patients is the development of confusion or coma precipitated by gastrointestinal bleeding, acute superimposed hepatitis, or concomitant infection in a previously asymptomatic patient with cirrhosis. The neurologic manifestations are mainly due to shunt of blood arising from the portal venous bed into the systemic circulation and are reversible once the liver function abnormality or precipitating factor has been corrected. HE can be classified according to the underlying liver disease and the evolution of the neurologic manifestations (Table 1). Clinical FeaturesClinically, HE manifests as a neuropsychiatric syndrome encompassing a wide spectrum of mental and motor disorders.2,3 The changes in mental status range from subtle cognitive dysfunction to severe coma, whereas the...

Rifaximin is an efficacious treatment for the parkinsonian phenotype of hepatic encephalopathy

“…None of the patients had any change in their ammonia level or EEG despite resolution of symptoms. MRI brain post-rifaximin in these patients showed reduction of the high T1 signal in the globus pallidus, imaging features classically associated with Parkinsonism in cirrhosis 5 (Fig. 1).…”

Espectroscopia cerebral em candidatos a transplante hepático

“…Estudos utilizando TNPS, EEG e espectroscopia têm demonstrado que disfunções cognitivas (EH leve ou subclínica) são comuns em pacientes portadores de hepatopatia crônica com função mental aparentemente normal ao exame clínico 5,15,[22][23][24][25] .…”

“…Recentemente, refinamentos técnicos na espectroscopia por ressonância magnética (RM) tornaram possível o estudo bioquímico do cérebro humano in vivo, com a identificação e quantificação dos metabólitos cerebrais em regiões específicas 4,8,22,29 . A encefalopatia hepática é caracterizada por depleção do mio-inositol (MI) e da colina (Cho) associada a um aumento do complexo glutamino-glutamato (Glx).…”

Multimodal brain monitoring in fulminant hepatic failure

“…However, the absence of these findings does not exclude the presence of brain swelling [22] , which may be better visualized through magnetic resonance imaging (MRI) of the brain [21] . The imbalance in the homeostasis of cell volume consequent to elevation of cerebral ammonia concentration can be disclosed in MRI by the proton spectroscopy findings of decreased myoinositol and choline signals [23] . Moreover, magnetization transfer ratio measurements of fast fluidattenuated inversion recovery sequences and diffusion weighted images can be used to detect abnormalities in white matter, thereby reflecting elevated ammonia concentrations in the central nervous system that facilitate the diagnosis of brain swelling in patients with FHF [23,24] .…”