A long series of toxic and metabolic disorders, acquired or inherited, may cause parkinsonian symptoms and signs (72). Many times the diagnosis is straightforward, known from the medical history, but the support of imaging studies may be useful in defining at least the extent of damage. This is the case of post-anoxic encephalopathy or carbon monoxide intoxication, in which the lesions involve the white matter and the basal ganglia where they are prevalent in the pallida (73,74). The same prevalent pallidal location is seen in cyanide intoxication (75). In other conditions, such as the unusual parkinsonian presentation of Wilson's disease, the correct diagnosis may be unsuspected and MRI, by demonstrating putaminal and lateral thalamic abnormalities or more extensive basal ganglia and brainstem involvement (25), may orient the diagnostic work-up to a rapid conclusion.
One condition in which MRI may suggest the correct diagnosis is manganese intoxication. This is manifested by hyperintensity in T1-weighted images in the pallida, sometimes extending caudally to the substantia nigra. Manganese accumulates in the pallida in many conditions, including liver cirrhosis with portacaval shunt and hepatic encephalopathy (76,77), long-term parenteral nutrition (78), environmental exposure in miners or industrial workers (79), or in other less clear conditions (80). Therefore, demonstration of pallidal hyperintensities in T1-weighted images should prompt investigations of blood manganese concentrations (Fig. 7).
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