Table 2.

Differential diagnosis table for basal ganglia signal abnormalities

Entity	Imaging Findings: MRI	Imaging Findings: CT	Clinical Findings
Physiologic calcification, normal variant [15]	Bilateral T1-hyperintense BG, GP more than putamen	CT: Calcifications in same distribution as MR	Seen as normal variant aging brain, asymptomatic Typically in patients older than 30 years
Manganese toxicity in long term total parenteral nutrition [9]	Bilateral T1-hyperintensity in the substantia nigra and GP, T2-unremarkable	CT: Unremarkable	History of long term total parenteral nutrition Findings secondary to manganese deposition
Disorders of calcium metabolism [16–17]	Bilateral T1-hyperintensity BG, T2-hypointense, SWI-blooming	CT: Bilateral BG calcifications	History of 1° or 2° hyperparathyroidism, 1° or 2° hypoparathyroidism, or pseudo-hypoparathyroidism
Chronic liver disease [18–19]	Bilateral T1-hyperintense BG (especially GP), pituitary	MR: Bilateral T1- hyperintense BG (especially GP), pituitary gland, and hypothalamus CT: Unremarkable	History/stigmata of chronic liver disease May present acutely with jaundice, encephalopathy
Wilson disease [20]	T1 BG signal variable, typically reduced, but may be hyperintense T2 “face of giant panda sign” normal red nucleus on background of hyperintense tegmentum	MR: T2 “face of giant panda sign” normal red nucleus on background of hyperintense tegmentum Widening of frontal horns, diffuse brain atrophy +/− BG hypodensity	T1 hyperintensity secondary to deposition of copper Liver disease, Kayser-Fleischer rings Decreased ceruloplasmin
Fahr disease [21–22]	BG T1 hyperintense, T2 variable, SWI-markedly hypointense	CT: Extensive symmetric BG calcifications (especially GP), thalami, cerebellum (dentate nuclei)	Neuropsychiatric disturbance, cognitive impairment, extrapyramidal findings Laboratory values normal
Hypoxic brain changes [23–24]	BG and cortical hyperintense lesions, DWI-restricted diffusion if acute	CT: If acute, normal After acute phase, decreased bilateral BG attenuation	History of anoxia, near-drowning, hypoxia, and/or cerebral hypoperfusion injury
Neurofibromatosis type one [25–26]	Foci of T1 and T2 hyperintensity in the deep gray nuclei (especially GP), may resolve by adulthood	CT?: BG unremarkable; optic or parenchymal gliomas may be present; sphenoid wing dysplasia	Cutaneous café au lait spots earliest finding Progressive vision loss due to optic gliomas Half of patients have macrocephaly