Cognitive and Behavior Deficits in Parkinson's Disease with Alteration of FDG-PET Irrespective of Age

Abstract

Significant progress has been made in our understanding of the neurobiology of Parkinson's disease (PD). Post-mortem studies are an important step and could help to comprehend not only the progression of motor symptoms, but also the involvement of other clinical domains, including cognition, behavior and impulse control disorders (ICDs). The correlation of neuropathological extension of the disease with the clinical stages remains challenging. Molecular imaging, including positron emission tomography (PET) and single photon computed tomography (SPECT), could allow for bridging the gap by providing in vivo evidence of disease extension. In the last decade, we have observed a plethora of reports describing improvements in the sensitivity of neuroimaging techniques. These data contribute to increasing the accuracy of PD diagnosis, differentiating PD from other causes of parkinsonism and also obtaining a surrogate marker of disease progression. FDG-PET has been used to measure cerebral metabolic rates of glucose, a proxy for neuronal activity, in PD. Many studies have shown that this technique could be used in early PD, where reduced metabolic activity correlates with disease progression and could predict histopathological diagnosis. The aim of this work is to report two particular cases of PD in which the assessment of brain metabolic activity (from FDG-PET) has been combined with clinical aspects of non-motor symptoms. Integration of information on neuropsychological and metabolic imaging allows us to improve the treatment of PD patients irrespective of age.

Keywords: 18F-FDG-PET; ICDs; Parkinson’s disease; dopamine agonists; molecular imaging.

Figure 1

Brain SPECT with 123 I-iofuplain (DaTSCAN).

Figure 2

Brain PET with 18F-FDG. Images highlight brain regions consistently found the analysis (Statistical Parametric Mapping software SPM 5 (p = 0.05). Diffuse hypometabolism in the left middle temporal gyrus, right and left inferior frontal gyrus, left middle frontal gyrus, left posterior cingulate, left inferior parietal lobule, right lentiform nucleus (putamen), right caudate head, left thalamus, left parahippocampal gyrus, right red nucleus (midbrain), left cerebellum pyramis, right and left cerebellum inferior semi-lunar lobule, right and left cerebellum posterior lobe tuber, right cerebellum anterior lobe nodule, left cerebellar tonsil.

Figure 3

Brain PET with 18F-FDG. Images highlight brain regions consistently found the analysis (Statistical Parametric Mapping software SPM 5 (p = 0.05). Hypometabolism in the left caudate body and head, left middle temporal gyrus, left superior temporal gyrus, right superior frontal gyrus, left and right inferior parietal lobule, left and right cerebrum sub-lobar insula, left and right superior temporal gyrus, left and right inferior frontal gyrus, right sub-lobar extra-nuclear gray matter, right cerebellar tonsil, right inferior temporal gyrus, left and right middle temporal gyrus, left limbic lobe uncus, left limbic lobe parahippocampal gyrus, right transverse temporal gyrus.