Manganese poisoning

Toxicosis

General description

Manganism, or manganese poisoning, is a neurological disorder caused by chronic exposure to excessive levels of manganese (Mn), commonly encountered in occupational settings such as welding. Manganese physiologically accumulates in the brain, particularly in regions like the basal ganglia, including the globus pallidus, caudate nucleus, putamen, and substantia nigra, as well as in the cerebral cortex and white matter. Inhaled manganese from the lungs enters the bloodstream, where it can quickly reach the brain and deposit, especially in the globus pallidus, if exposure levels are high.

Early symptoms of manganism often involve psychiatric and behavioral changes, such as slowed response, irritability, mood swings, and compulsive behavior. With continued exposure, neurological symptoms resembling Parkinson’s disease emerge, including bilateral motor symptoms, dystonia, postural instability, and action tremors. However, manganism can be distinguished from Parkinson’s disease by its rapid progression, poor response to L-Dopa treatment, and unique presentation, often leading to a faster decline in motor function and higher rates of dystonia and postural reflex issues.

Radiographic features

MRI shows symmetric bilateral T1WI hyperintensity primarily in the globus pallidus, with similar signal changes occasionally extending to the putamen, dentate nuclei, corpus callosum, and cerebral white matter in severe cases. Additional signal changes may also be observed in the substantia nigra, tegmentum of the pons, and anterior lobe of the pituitary gland.

T1WI hyperintensity

  • Globus pallidus
  • Putamen
  • Dentate nucleus
  • Corpus callosum
  • Cerebrum
    Cerebral white matter
  • Substantia nigra
  • Brainstem
    Pons
    Pontine tegmentum
  • Pituitary gland
    Anterior pituitary
Symmetric
Bilateral
T1WI
Hyperintensity