Abstract
A 70-year-old woman developed marked akinesia after an anoxic event related to bronchiectasia. Magnetic resonance imaging studies revealed lesions in the bilateral globus pallidus and, to a lesser extent, in the putamen. Positron emission tomography studies with (18)F-6-fluoro-L-dopa and (11)C-N-methylspiperone showed a decreased pre- and post-synaptic uptake in the striatum. Consistent with previous reports, the present case demonstrated the basal ganglia, particularly the globus pallidus, to be selectively susceptible to anoxic insults. Furthermore, a PET study indicated a disrupted presynaptic integrity of the dopaminergic terminals and decreased dopamine D(2) receptor binding, which together appear to underlie the pathophysiology of post-anoxic akinesia, at least in the present case.
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