Basal ganglia T1 hyperintensity

There are many causes of basal ganglia T1 hyperintensity, but the majority relate to deposition of T1-shortening elements within the basal ganglia such as:

• calcium

  • idiopathic calcification

  • calcium and phosphate abnormalities

• hepatic dysfunction or bypass (specifically affecting globi pallidi)

  • acquired non-Wilsonian hepatocerebral degeneration

  • Wilson disease (copper)

  • hepatic encephalopathy

  • hereditary hemorrhagic telangiectasia, often with hepatic arteriovenous malformations ⁵

• toxins/ischemia

  • carbon monoxide (usually low T1 signal; unless associated with hemorrhage)

  • hyperalimentation or long term parenteral nutrition (manganese)

  • hyperglycemia-associated choreaballism ²: non-ketotic hyperglycemic hemichorea (NHH)

  • previous administration of linear gadolinium chelates ^3,4

  • global hypoxia

• blood

  • methemoglobin in intracranial hemorrhage

  • hemorrhagic infarct

• others

  • Japanese encephalitis

  • hamartoma in neurofibromatosis type 1

  • Fabry disease

  • hypermanganesemia with dystonia 1

  • hypermanganesemia with dystonia 2

See also

• basal ganglia signal abnormalities

  • increased T2 signal in the basal ganglia

  • decreased T2 signal in the basal ganglia

  • decreased T1 signal in the basal ganglia

  • restricted diffusion in the basal ganglia

• basal ganglia calcification

• eye of tiger sign