Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An [¹⁸F]Fluorodeoxyglucose Positron Emission Computed Tomography Study

Abstract

Aim: We sought to identify markers of motor and nonmotor function in Parkinson's disease (PD) using advanced neuroimaging techniques in subjects with PD. Methods: We enrolled 26 nondemented PD subjects and 12 control subjects. All subjects underwent [¹⁸F]fluorodeoxyglucose positron emission computed tomography (FDG-PET) and magnetic resonance imaging, and a complete neuropsychological battery. Results: FDG-PET of subjects with PD revealed significant metabolic elevations in the bilateral posterior lentiform nucleus, posterior cingulate, and parahippocampus, and metabolic reductions in the bilateral temporoparietal association cortex and occipital lobe versus controls. PD subjects had significant reductions in executive/attention function, memory/verbal learning, and speed of thinking, and significantly increased depression, anxiety and apathy scores compared with controls. Motor dysfunction correlated with increased metabolism in the posterior lentiform nucleus, pons, and cerebellum, and decreased metabolism in the temporoparietal lobe. Cognitive dysfunction correlated with increased posterior cingulate metabolism and decreased temporoparietal lobe metabolism. Depressive symptoms correlated with increased amygdala metabolism; anxiety scores correlated with decreased caudate metabolism, and apathy scores correlated with increased metabolism in the anterior cingulate and orbitofrontal lobe and decreased metabolism in the temporoparietal association cortex. Conclusions: Our findings showed that motor, cognitive, and emotional dysfunction in PD are associated with distinct patterns of cerebral metabolic changes.

Depression, anxiety, and apathy in Parkinson's disease: insights from neuroimaging studies

“…Studies using T1‐weighted imaging reported reduced GM thickness in the temporal lobes 62 or increased atrophy in the frontal and parietal lobes (e.g. bilateral precentral gyri, right precuneus and posterior cingulate cortex), insula 63 and left nucleus accumbens 65 to be correlated with apathy, although this was not replicated in other studies 14, 64. The only study using DTI to examine the neural substrates of apathy in PD did not observe any difference in white matter integrity between patients with apathy and those without apathy and HCs 65.…”

“…However, positive correlations between apathy and prefrontal, temporal, parietal and limbic areas were also noted in some studies 14, 56, 57, 58. Studies using T1‐weighted imaging reported reduced GM thickness in the temporal lobes 62 or increased atrophy in the frontal and parietal lobes (e.g.…”

“…The remaining four of the 38 studies reported findings from structural T1‐weighted imaging plus another imaging method, including PET 14, DTI 45, task FMRI 46 and RS‐FMRI 47, respectively. One study performed both TCS and T2‐weighted MRI 48.…”

Apathy in Parkinson's disease: clinical features, neural substrates, diagnosis, and treatment

“…2 Several functional imaging studies 94,95 in patients with Parkinson's disease without dementia have supported this hypothesis, showing that these patients can present with abnormal activation at the level of the dorsolateral or ventrolateral prefrontal cortex and caudate nucleus during executive tasks. Results from glucose metabolism studies [96][97][98] with ¹⁸F-FDG PET in Parkinson's disease have shown that apathy severity is associated with metabolic activity in diff erent cognitive regions, including the inferior medial frontal gyrus, cingulate cortex, insula, cuneus, and tempo roparietal region.…”

Nuclear Medicine Applications in Movement Disorders

“…Parkinsonizm sendromlarında beyin FDG PET görüntüleme saptanan anormal bulguların yaygınlığı ve derecesi klinik bulgular ile genellikle korelasyon gösterir (1,3,19,23,24,30,34,35,39,49,50,51,52). PH için klinik belirtiler ile ilişkili özgül metabolik tutulum biçimleri bulunur: Örneğin; tremor ile ilişkili serebellotalamo-kortikal yolakların etkilendiği (23,31,53); motor belirtiler ile ilişkili olarak putamen ve premotor korteksi içine alan (19,50,52,53); bilişsel bozukluklar ile ilişkili olarak da frontal ve parietal asosiyasyon alanlarında hipometabolizma ve serebellumda hipermetabolizma ile karakterize özgül metabolik ağ yapıları tanımlanmıştır (53,54).…”