Structural MRI changes
The radiological presentation of the disease strongly depends on the acuteness of the process. In patients with liver cirrhosis and chronic encephalopathy, the most characteristic feature on T1-weighted images (T1WI) is a bilateral and symmetric increase in signal intensity (hyperintensity).
The changes are predominantly localized in the basal ganglia, specifically involving the globus pallidus. An important feature of this MRI pattern is its potential reversibility: clinical observations confirm that following successful liver transplantation, the signal in the globus pallidus completely normalizes.
Proton MR spectroscopy
Single-voxel proton MR spectroscopy is used for a deep assessment of metabolic disorders. Measurements are usually performed in the parietal region, encompassing visually unremarkable white matter.
Key metabolites and their resonant frequencies:
- NAA (N-acetylaspartate) — 2.0 ppm. Acts as a marker of neuronal integrity.
- Glx (glutamine/glutamate) — 2.1–2.5 ppm.
- Cr (creatine/phosphocreatine) — 3.02 ppm.
- Cho (choline-containing compounds) — 3.2 ppm.
- mIns (myo-inositol) — 3.55 ppm.
Dynamics of changes: Before surgery, the spectrum demonstrates a sharp increase in the Glx peak, accompanied by a drop in the concentration of mIns and Cho. Meanwhile, the NAA level remains within normal limits, indicating that the neurons themselves are preserved. Following liver transplantation, the balance of metabolites (Glx, mIns, Cho) completely recovers to normal values.
Acute hepatic encephalopathy
The development of acute hepatic encephalopathy (Acute Hepatic Encephalopathy) requires the analysis of additional MR sequences, such as diffusion-weighted imaging (DWI / DWI), apparent diffusion coefficient maps (ADC maps / ADC maps), as well as T2WI and T2-FLAIR.
Tomograms reveal bilateral hyperintense lesions affecting:
- The cortical grey matter of the temporal and frontal lobes, as well as the insular cortex;
- The thalami;
- The dorsal brainstem.
Key diagnostic criterion of the acute phase is the presence of restricted diffusivity (restricted diffusivity). Pathological areas appear bright on DWI and are confirmed by a dark signal on ADC maps.
Differential diagnosis of metabolic lesions
The MRI presentation of liver dysfunction must be differentiated from other types of metabolic encephalopathies:
- Hypoglycemic encephalopathy: Also characterized by diffusion restriction, but the lesions are localized in the cortical grey matter, deep brain nuclei, and, most importantly, symmetrically affect both hippocampi.
- Non-ketotic hyperglycemia: Demonstrates a completely different pattern. In this case, T2WI and T2-FLAIR visualize hypointense (dark) lesions typically located in the right occipital subcortical white matter.
MR spectroscopy rationale: in liver failure, excess ammonia in the brain is converted into glutamine (Glx ↑). To prevent osmotic edema, neurons expel myo-inositol (mIns ↓). The cells themselves do not die, which is why NAA remains normal.
Class and exam questions
What is the T2-FLAIR mode and why is it needed?
FLAIR (Fluid-attenuation inversion recovery) is an inversion recovery pulse sequence in which the signal from free fluid (e.g., cerebrospinal fluid) is software-suppressed. This provides enhanced contrast for visualizing lesions in the brain parenchyma near the ventricles and sulci.
Are neurons preserved in hepatic encephalopathy?
Yes, neuronal integrity is preserved. This is confirmed by the stable level of the N-acetylaspartate (NAA) marker on MR spectroscopy both before and after treatment.
In which brain structure should changes be sought on T1WI outside of an exacerbation?
The most typical localization of chronic changes in liver dysfunction is the globus pallidus. A bilateral symmetric increase in the MR signal is detected in this zone.
What else to study on this topic
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- Neuroimaging in CNS vasculitis and systemic lupus erythematosus (including antiphospholipid syndrome).
- Specific syndromes: CLIPPERS syndrome and acute disseminated encephalomyelitis (ADEM).
- Pattern recognition in adult genetic leukoencephalopathies and reversible cerebral vasoconstriction syndrome (RCVS).
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