Hepatic Encephalopathy MRI

Sagittal and Axial T1 images show bilateral symmetrical hyperintensity in the region of Globus pallidi in a pt with altered sensorium and chronic liver disease suggestive of Hepatic Encephalopathy.

Syn : Hepatic coma.
A potentially reversible clinical syndrome seen in patients with acute or chronic liver disease.
CT study of brain is often normal.
MRI is investigation of choice. Bilateral basal ganglionic faint T1 hyperintensity particularly in the region of Globus pallidi is an imagingwise diagnostic clue.
May see an associated increased signal in pituitary, hypothalamus, and mid brain or it may the only abnormality particularly in childhood liver disease.

Histopathological studies have reported degenerative changes of astrocytes followed by neuronal damage. Focal cytotoxic odema in the involved area. No inflammatory infiltrates or demyelination.

Etiology:
Liver cirrhosis, Acute Fulminant viral hepatitis.
Drugs and toxins.
Shock and sepsis.
Porto systemic shunting.
Accumulation of neurotoxins like Ammonia, manganese, aromatic amino acids; Bilirubin;  neuroactive drungs used as sedative in pts with liver disease.

HE occur in ~50% cases of liver cirrhosis. HE is precipited by ammoniagenic situations like oral protein load, GI hemorrhage and Constipation.

Clinical features:
Reported at any age with no gender predominance.
Altered mental status - stumor and comma.
Jaundice, Palmar erythema, Spider angiomata,
Motor – tremor, bradykinesia, asterixis, ataxia, apraxia,
May show associated Parkinsonian signs.

DDs of hyperintense Globus pallidi on T1:
Hepatic / Bilirubin Encephalopathy.
Hyperglycemia.
Manganese accumulation.