Giusy Caiazzo (Italy)
Università degli studi della Campania "Luigi Vanvitelli" Department of Advanced Medical and Surgical SciencesAuthor Of 2 Presentations
INTRINSIC BRAIN FUNCTIONAL CONNECTIVITY PREDICTS TREATMENT-RELATED MOTOR COMPLICATIONS IN EARLY PARKINSON’S DISEASE PATIENTS
- Rosa De Micco (Italy)
Abstract
Background and Aims:
Dopamine replacement therapy (DRT) is the most effective treatment for patients with Parkinson’s disease (PD). However, DRT is complicated by the evolution of treatment-related motor complications which may develop progressively over the disease course. Using resting-state functional MRI, we investigated intrinsic brain networks connectivity at baseline in a cohort of drug-naïve PD patients which successively developed treatment-related motor complications over a 4-year follow-up period compared with patients who did not.
Methods:
Baseline 3Tesla MRI images of 88 drug-naïve PD patients and 20 healthy controls (HC) were analyzed. At the 4-year follow-up, 35 patients have developed treatment-related motor complications (PD-Comp) whereas 53 had not (PD-no-Comp). Single-subject and group-level independent component analysis was used to investigate functional connectivity changes within the major resting-state networks at baseline. Additionally, a region-of-interest analysis was performed within the basal ganglia. Sex and age were run as covariates. Regression analysis was used to investigate baseline predictors of motor complications development.
Results:
At baseline, PD-Compl patients showed a preserved sensorimotor connectivity compared to HC. Moreover, an increased connectivity within the default-mode and the frontoparietal networks as well as within the basal ganglia were detected in PD-Compl compared with PD-no-Compl. Functional connectivity changes at baseline showed to be an independent predictor of motor complications after 4 years.
Conclusions:
Our findings demonstrated that specific functional connectivity changes may characterize drug-naïve PD patients more prone to develop treatment-related complications. We hypothesize that these findings may reflect the presence of early differences within the dopaminergic pathways and might predict development of motor complications over time.
DISCONNECTOME OF THE MIGRAINE BRAIN: A MODEL OF MIGRAINE AS “CONNECTOPATHY”
- Marcello Silvestro (Italy)
Abstract
Background and Aims:
The structural substrates enabling functional communications among brain connectome, characterized by high stability and reproducibility, have not been investigated in migraine by means of graph analysis approach.
We hypothesize that a rearrangement of the brain connectome with an increase of both strength and density of connections between cortical areas involved in pain perception, processing and modulation may characterize migraine patients.
Methods:
We investigated, using high angular resolution diffusion-weighted MRI imaging tractography-based graph analysis, the graph-topological indices of the brain “connectome”, a set of grey matter regions (nodes) structurally connected by white matter paths (edges) in 94 patients with migraine without aura compared with 91 healthy controls.
Results:
We observed in migraine patients: i) higher local and global network efficiency (p< 0.001) and ii) higher local and global clustering coefficient (p< 0.001). Moreover, we found changes in the hubs topology in migraine patients: i) posterior cingulate cortex and inferior parietal lobule assuming the hub role and ii) fronto-orbital cortex, involved in emotional aspects, and the visual areas, involved in migraine pathophysiology, losing the hub role. Finally, we found a higher connection probability (edges) between cortical nodes involved in pain perception as well as in cognitive and affective attribution of pain experiences, in migraine patients (p< 0.001).
Conclusions:
The imbalance between the need of investing resources to promote network efficiency and the need of minimizing the metabolic cost of wiring probably represents the mechanism underlying migraine patients’ susceptibility to triggers. Such change in connectome topography suggest an intriguing pathophysiological model of migraine as brain “connectopathy”.