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Table 1.  

Differential Imaging Findings in Parkinsonian Syndromes

Table 2.  

Differential Imaging Findings in Dementias

Technology Insight: Imaging Neurodegeneration in Parkinson's Disease: Serotonergic, Noradrenergic and Cholinergic Function


Serotonergic, Noradrenergic and Cholinergic Function

In PD, there is loss of not only dopaminergic projections, but also serotonergic, noradrenergic and cholinergic projections. The median raphe and locus ceruleus both contain aromatic amino-acid decarboxylase and so can take up and store 18F-dopa, a process that gives an indirect insight into the functional integrity of the seroton ergic and noradrenergic systems. It has been reported that 18F-dopa uptake in the median raphe is initially elevated in PD but later falls below normal as the disease advances. 18F-dopa uptake in the locus ceruleus is normal in early PD but falls at the end stage of the disease.[35] A more direct measure of serotonergic function is provided by use of 11C-WAY-100635 PET to quantify 5-HT1A receptor binding potential in the median raphe. One series in patients with PD showed a mean 25% loss of 5-HT1A binding in the median raphe, which correlated with the severity of resting tremor but not with rigidity or bradykinesia.[36] These data suggest that midbrain tegmentum pathology might be relevant to the etiology of PD tremor.

Interestingly, no correlation between serotonergic dysfunction and depressive symptoms has been detected in patients with PD,[37] but there is evidence that dysfunction of noradrenergic and limbic monoaminergic projections is asso ciated with depression. Patients with both PD and depression, when compared with patients who have equivalent disability but not depression, have been reported to show decreased levels of 11C-RTI 32 uptake (a marker of norepinephrine [noradrenaline] and dopamine terminal function) in the thalamus and locus ceruleus, which probably reflects reduced noradrenergic input, along with lower signals in the limbic areas (amygdala and ventral striatum).[38]

Cholinergic function can be assessed pre synaptically with 123I-benzovesamicol, a SPECT marker of vesicular acetylcholine transporter binding. In patients who have PD without dementia, there is a significant reduction of 123I-benzovesamicol binding in the parietal and occipital lobes only, whereas patients with PDD show globally reduced 123I-benzovesamicol binding.[39] Both N-11C-methyl-4-piperidyl acetate (11C-MP4A) PET and N-11C-methylpiperidin-4-yl propionate 11C-PMP PET can be used to measure acetylcholinesterase levels. Hilker and colleagues performed 11C-MP4A and 18F-dopa PET studies in 17 patients with PD and 10 patients with PDD.[40]11C-MP4A binding in the cortical regions was reduced by 10% in the patients with PD and by 29.7% in the patients with PDD when compared with controls. The individual levels of striatal 18F-dopa uptake correlated with 11C-MP4A binding in the cortical regions, which suggests a simultaneous loss of both transmitters. The findings reported with 11C-PMP PET scans in patients with PD or PDD parallel those of 11C-MP4A PET scans in these patients.[41] Loss of cholinergic function is likely to be an important contributory factor to the dementia process in PD, as levels of cortical acetylcholinesterase in PD have been shown to correlate with performance on attentional and working memory tasks.[42]

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