Reduced but fluctuating conscious state following recent admission for sepsis. No abnormality on CT brain. Encephalitis?
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The caudate and lentiform nuclei, particularly on the right, demonstrate high T2 signal, with minor T2 shine through but no convincing abnormal diffusion restriction.
Mild asymmetry in FLAIR signal in the left anterior temporal lobe without mass effect may be related to artifact or the large traversing developmental venous anomaly (DVA) - best seen on coronal T1 C+.
Mild asymmetric susceptibility in the left lentiform nucleus compared to the right. However, the T1 hyperintensity in the left globus pallidus is symmetric. Correlation with the CTB show that there is no calcification.
In the anterior right middle cranial fossa is a durally-based avidly enhancing lesion touching the anterior temporal lobe without adjacent FLAIR hyperintensity consistent with a meningioma.
Scattered foci of periventricular and deep white matter T2 FLAIR high signal most likely reflect sequelae of chronic small vessel ischaemia.
Presence of intrinsic high T1 signal in the basal ganglia raised the possibility of underlying acquired hepatocerebral degeneration with superimposed hepatic encephalopathy accounting for T2 signal abnormality and clinical presentation. At the time no history of liver disease was present however.
Recent blood work revealed elevated ammonia levels at 100 umol/L (normal <55 umol/L), and deranged liver function tests.
In the setting of suspected hepatic encephalopathy, the patient went on to have an ultrasound which demonstrated imaging findings of cirrhosis without ultrasound evidence of portal hypertension. Both ARFI (shear wave elastography) measurement sets are in the cirrhotic range.
The patient was managed medically and mental state returned to normal.