Basal ganglia neurotoxins

The epidemiology, clinical features, pathology, and mechanisms of action of basal ganglia neurotoxins are reviewed. Manganese, cyanide, hydrogen sulfi de, methanol, carbon monoxide, 3-nitropropionic acid, MPTP, and annonaceae alkaloids are discussed. The probable mechanism of action for almost all ba sal ganglia neurotoxins is inhibition of mitochondrial function with destru ction of the pallidum and putamen. MPTP produces selective loss of dopamine rgic neurons because of selective uptake of a toxic metabolite in dopaminer gic neurons. The basis for selective vulnerability of the putamen and palli dum is unknown.