There are a limited number of causes of hyperintensity within the basal ganglia on T1-weighted magnetic resonance (MR) images (T1WI) without correlates on CT or T2 weighted sequences. This finding is most commonly seen in patients who have chronic liver disease or who are on parenteral nutrition. In parenteral nutrition, it is thought to be due to the deposition of trace elements such as manganese, mainly in the globi pallidi and subthalamic nuclei, and/or reaction to these elements. These findings have been shown to regress on follow-up imaging one year following cessation of manganese administration. In patients with chronic liver disease, increased signal is seen in the globus pallidus and portions of the internal capsules and cerebral peduncles. Increased signal has been described in patients with cirrhosis and portal-systemic collaterals receiving blood from an enlarged superior mesenteric vein. While the signal abnormality is essentially on T1WI, abnormalities can also be seen on the proton density images due to the contribution from T1 shortening.

Although rare, acute chorea-ballism associated with hyperglycemia also demonstrates hyperintensity on T1WI without abnormality on T2-weighted MRI (T2WI). In hemorrhage, the hyperintensity on T1WI is thought to be due to methemoglobin. In etiologies such as evolving infarct, hemorrhage, Wilson’s disease, and encephalitis, there is associated abnormality on the T2WI. There is associated hyperattenuation on CT in patients with hemorrhage and calcification, and hypoattenuation is present in other etiologies such as encephalitis, Wilson’s disease, neurofibromatosis, or hypoxic-ischemic encephalopathy.