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Home arrow Computer Science arrow Computational Diffusion MRI: MICCAI Workshop, Athens, Greece, October 2016
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Introduction

SWEDD or (scans without evidence of dopaminergic deficit) are a group of clinically diagnosed patients with Parkinson symptoms who reveal no evidence of dopaminergic deficit on [123I] FP-CIT Single Photon Emission Computerized Tomography (SPECT) which is identified as marker of disease progression [1,2]. The true entity of patients with Parkinsonism as with SWEDD is still unknown. While SWEDD patients were first identified following entrance and follow up DAT Scanning of patients with assumed Parkinson disease (PD), there is propensity to classify SWEDD patients as a distinct disorder in that they do not show imaging progress toward PD and do not respond to classical levodopa treatment [3]. Additionally studies have shown that PD is clinically over diagnosed in uncertain cases therefore misdiagnosis of this group might expire a golden time for initiation of a proper treatment. In fact a longitudinal follow up of patients with DAT imaging within normal range has revealed that in up to 44% of these patients the initial diagnosis changes to other disorders not associated with DAT deficit or PD. These patients also exhibit lower Unified Parkinson’s Disease Rating Scale (UPRDS) score which remain relatively constant during the course of disease [4]. Another study demonstrated that the arm tremor pattern in SWEDD group as well as their response to PMS conditioning along with their minimal responsiveness to dopaminergic therapy can clinically discriminate between them and PD patients [5]. The occurrence of focal or segmental dystonia and task specificity of dystonia. Lack of true bradykinesia and absence of the non-motor symptoms of PD also favors the diagnosis of SWEDD rather than PD [6]. Furthermore emerging evidence of differential DAT scan quantification parameters and patterns in PD group vs. normal and SWEDD group [7] are being provided whereas little data exist on the specific regional involvement of extranigral or cortical areas that might help determine the true nature of SWEDD group and facilitate clinical judgment between SWEDD and PD group and adult onset dystonia which often exhibits overlapping clinical and experimental features with SWEDD [5].

The cingulate gyrus is a major white matter tract with implications in emotion formation and executive function and also plays a major role in cognitive control of limbic lobe functions such as response initiation. Cingulate gyrus also works in close functional and structural relation with prefrontal cortex and its adjacent dorsal anterior cingulate cortex to maintain an intact executive function [8] and connecting sites with known role in cognitive control. Decreased FA is observed in cingulum of PD patients in both demented and early-stage non-demented patients. Contrary to FA, the increase in mean diffusivity in early stages of PD compared to normal controls is associated with better performance in semantic fluency and other cognitive tasks in newly diagnosed PD patients [9, 10]. The anterior and posterior cingulum microstructure and function differ in which each convey different cortical connections to the prefrontal and parieto-occipital cortices respectively [8]. This can explain their role in task set/verbal memory loss (rostral part of cingulum) and visuospatial memory impairment (parahippocampal Cingulum) in PD [11].

 
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