Abstract Aim The aim of the present study is to investigate the relations between both functional connectivity and brain networks with cognitive decline, in patients with Parkinson’s disease (PD). Introduction PD phenotype is not limited to motor impairment but, rather, a wide range of non-motor disturbances can occur, cognitive impairment being one of the commonest. However, how the large-scale organization of brain activity differs in cognitively impaired patients, as opposed to cognitively preserved ones, remains poorly understood. Methods Starting from source-reconstructed resting-state magnetoencephalography data, we applied the PLM to estimate functional connectivity, globally and between brain areas, in PD patients with and without cognitive impairment (respectively PD-CI and PD-NC), as compared to healthy subjects (HS). Furthermore, using graph analysis, we characterized the alterations in brain network topology and related these, as well as the functional connectivity, to cognitive performance. Results We found reduced global and nodal PLM in several temporal (fusiform gyrus, Heschl’s gyrus and inferior temporal gyrus), parietal (postcentral gyrus), and occipital (lingual gyrus) areas within the left hemisphere, in the gamma band, in PD-CI patients, as compared to PD-NC and HS. With regard to the global topological features, PD-CI patients, as compared to HS and PD-NC patients, showed differences in multi frequencies bands (delta, alpha, gamma) in the Leaf fraction, Tree hierarchy (both higher in PD-CI) and Diameter (lower in PD-CI). Finally, we found statistically significant correlations between the MoCA test and both the Diameter in delta band and the Tree Hierarchy in the alpha band. Conclusion Our work points to specific large-scale rearrangements that occur selectively in cognitively compromised PD patients and correlated to cognitive impairment.
Functional motor disorders (FMD) are a frequent neurological condition affecting patients with movement disorders. Commonly described in younger adults, their manifestation can be also associated to an elderly onset.
Abstract Background Despite its clinical relevance, the pathophysiology of pain in Parkinson's disease (PD) is still largely unknown, and both central and peripheral mechanisms have been invoked. Objectives To investigate whether central pain processing is altered in “drug‐naive” pain‐free PD (dnPD) patients. Methods Using event‐related functional MRI (fMRI), functional response to forearm heat stimulation (FHS) at two different intensities (41°C and 53°C) was investigated in 20 pain‐free dnPD patients, compared with 18 healthy controls (HCs). Secondary analyses were performed to evaluate associations between BOLD signal changes and PD clinical features and behavioral responses. Results During low‐innocuous FHS (41°C), no activation differences were found between dnPD patients and HCs. During high‐noxious FHS (53°C) a significantly increased activation in the left somatosensory cortex, left cerebellum, and right low pons was observed in dnPD patients compared to HCs. In the latter experimental condition, fMRI BOLD signal changes in the right low pons ( p < .0001; R = −0.8) and in the cerebellum ( p = .004; R = −0.7) were negatively correlated with pain intensity ratings only in dnPD patients. No statistically significant difference in experimental pain perception was detected between dnPD patients and HCs. Conclusions Our findings suggest that a functional remodulation of pain processing pathways occurs even in the absence of clinically overt pain symptoms in dnPD patients. These mechanisms may eventually become dysfunctional over time, contributing to the emergence of pain symptoms in more advanced PD stages. The comprehension of pain‐related mechanisms may improve the clinical approach and therapeutic management of this disabling nonmotor symptom.
Background Migraine is a disabling neurological condition characterized by headache attacks, hypersensitivities to visual, auditory, olfactory and somatosensory stimuli, nausea and vomiting. Peripheral and central sensitization of trigeminovascular neurons seem to play a critical role in different aspects of migraine pathophysiology [1]. In the last years, several studies investigated pain thresholds in patients with migraine during both attacks and interictal periods. However, pain perception in patients with migraine has been poorly explored. Objective To investigate perception intensity of trigeminal heat stimulation (THS) [2] in patients with migraine without (MwoA CA-) and with allodynia (MwoA CA+) compared to healthy controls (HC) and correlation with clinical parameters of migraine severity. Methods We enrolled 80 patients with migraine (40 patients with MwoA CA- and 40 patients with MwoA CA+) and 60 HC. THS was performed using the contact heat evoked potential stimulator (CHEPS) at three different intensities: a low-innocuous stimulus at 41°C and two painful heat stimuli at 51° and 53°C (to provide a moderate-noxious and a high-noxious stimulus). Subjects had to verbally rate the intensity perception of the experimental stimulus by means of a numerical rating scale (NRS) ranging from 0( “no pain” )t o 10 (“worst pain imaginable”). Results NRS of pain perception was not significantly different between patients with MwoA (as a group) and HC at any level of experimental stimuli. The absence of significant differences in pain perception was also found between patient groups defined as patients with MwoA CA- and with MwoA CA+ compared to HC, at any level of experimental stimuli. Conclusions
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