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Zhao C.,Southwest University | Zhao C.,University of Manchester | Valentini E.,University of Rome La Sapienza | Valentini E.,Scientific Institute for Research | Hu L.,Southwest University
Experimental Brain Research | Year: 2014

Research on brain mechanisms of deviance detection and sensory memory trace formation, best indexed by the mismatch negativity, mainly relied on the investigation of responses elicited by auditory stimuli. However, comparable less research reported the mismatch negativity elicited by somatosensory stimuli. More importantly, little is known on the functional features of mismatch deviant and standard responses across different sensory modalities. To directly compare different sensory modalities, we adopted a crossmodal roving paradigm and collected event-related potentials elicited by auditory, non-nociceptive somatosensory, and nociceptive trains of stimuli, during Active and Passive attentional conditions. We applied a topographical segmentation analysis to cluster successive scalp topographies with quasi-stable landscape of significant differences to extract crossmodal mismatch responses. We obtained three main findings. First, across different sensory modalities and attentional conditions, the formation of a standard sensory trace became robust mainly after the second stimulus repetition. Second, the neural representation of a modality deviant stimulus was influenced by the preceding sensory modality. Third, the mismatch negativity significantly covaried between Active and Passive attentional conditions within the same sensory modality, but not between different sensory modalities. These findings provide robust evidence that, while different modalities share a similar process of standard trace formation, the process of deviance detection is largely modality dependent. © 2014, Springer-Verlag Berlin Heidelberg.

Hu L.,Southwest University | Peng W.,University of Hong Kong | Valentini E.,University of Rome La Sapienza | Valentini E.,Scientific Institute for Research | And 2 more authors.
Journal of Pain | Year: 2013

Nociceptive stimuli can induce a transient suppression of electroencephalographic oscillations in the alpha frequency band (ie, alpha event-related desynchronization, α-ERD). Here we investigated whether α-ERD could be functionally distinguished in 2 temporally and spatially segregated subcomponents as suggested by previous studies. In addition, we tested whether the degree of dependence of nociceptive-induced α-ERD magnitude on the prestimulus α-power would have been larger than the degree of dependence on the poststimulus α-power. Our findings confirmed the dissociation between a sensory-related α-ERD maximally distributed over contralateral central electrodes, and a task-related α-ERD (possibly affected by motor-related activity), maximally distributed at posterior parietal and occipital electrodes. The cortical sources of these activities were estimated to be located at the level of sensorimotor and bilateral occipital cortices, respectively. Importantly, the time course of the α-ERD revealed that functional segregation emerged only at late latencies (400 to 750 ms) whereas topographic similarity was observed at earlier latencies (250 to 350 ms). Furthermore, the nociceptive-induced α-ERD magnitude was significantly more dependent on prestimulus than poststimulus α-power. Altogether these findings provide direct evidence that the nociceptive-induced α-ERD reflects the summation of sensory-related and task-related cortical processes, and that prestimulus fluctuations can remarkably influence the non-phase-locked nociceptive α-ERD. Perspective: Present results extend the functional understanding of α-oscillation suppression during pain perception and demonstrate the influence of prestimulus variability on this cortical phenomenon. This work has the potential to guide pain clinicians in a more accurate interpretation on physiological and psychological modulations of α-oscillations. © 2013 by the American Pain Society.

Hu L.,Southwest University | Valentini E.,University of Rome La Sapienza | Valentini E.,Scientific Institute for Research | Zhang Z.G.,University of Hong Kong | And 2 more authors.
NeuroImage | Year: 2014

Nociceptive laser pulses elicit temporally-distinct cortical responses (the N1, N2 and P2 waves of laser-evoked potentials, LEPs) mainly reflecting the activity of the primary somatosensory cortex (S1) contralateral to the stimulated side, and of the bilateral operculoinsular and cingulate cortices. Here, by performing two different EEG experiments and applying a range of analysis approaches (microstate analysis, scalp topography, single-trial estimation), we describe a distinct component in the last part of the human LEP response (P4 wave). We obtained three main results. First, the LEP is reliably decomposed in four main and distinct functional microstates, corresponding to the N1, N2, P2, and P4 waves, regardless of stimulus territory. Second, the scalp and source configurations of the P4 wave follow a clear somatotopical organization, indicating that this response is likely to be partly generated in contralateral S1. Third, single-trial latencies and amplitudes of the P4 are tightly coupled with those of the N1, and are similarly sensitive to experimental manipulations (e.g., to crossing the hands over the body midline), suggesting that the P4 and N1 may have common neural sources. These results indicate that the P4 wave is a clear and distinct LEP component, which should be considered in LEP studies to achieve a comprehensive understanding of the brain response to nociceptive stimulation. © 2013.

Zucco F.,Presenza Amica Association | Bonezzi C.,Scientific Institute for Research | Fornasari D.,National Research Council Italy
Advances in Therapy | Year: 2014

Pain presents in 80% of patients with advanced cancer, and 30% have periods of increased pain due to fluctuating intensity, known as breakthrough cancer pain (BTcP). BTcP is high-intensity, short-duration pain occurring in several episodes per day and is non-responsive to treatment. The clinical approach to BTcP is variable. A review of the literature was performed to provide clinicians and practitioners with a rational synthesis of the ongoing scientific debate on BTcP and to provide a basis for optimal clinical approach to BTcP in adult Italian patients. Data show that circadian exacerbations of pain should be carefully monitored, differentiating, if possible, between fluctuations of background pain (BP), end-of-dose effect, and BTcP. BTcP should be monitored in all care contexts in clinical practice and each care facility must have all the medications and products approved for use in BTcP at their disposal. Data show that knowledge about medications for BTcP is lacking: medications for BTcP treatment are not interchangeable, although containing the same active substance; each physician must know the specific characteristics of each medication, its pharmacological properties, limitations in clinical practice, specifics relating to titration and repeatability of administration, and technical specifics relating to the accessibility and delivery. Importantly, before choosing a rapid-onset opioid (ROO), it is essential to deeply understand the status of patient and the characteristics of their family unit/caregivers, taking into account the patient's progressive loss of autonomy and/or cognitive-relational functionality. When BTcP therapy is initiated or changed, special attention must be paid to training the patient and family members/caregivers, providing clear instructions regarding the timing of drug administration. The patient must already be treated effectively with opioids before introducing ROOs for control of BTcP. © 2014 The Author(s).

van Dijk K.D.,VU University Amsterdam | Persichetti E.,University of Perugia | Chiasserini D.,University of Perugia | Chiasserini D.,VU University Amsterdam | And 7 more authors.
Movement Disorders | Year: 2013

Parkinson's disease (PD) is characterized neuropathologically by the cytoplasmic accumulation of misfolded α-synuclein in specific brain regions. The endolysosomal pathway appears to be involved in α-synuclein degradation and, thus, may be relevant to PD pathogenesis. This assumption is further strengthened by the association between PD and mutations in the gene encoding for the lysosomal hydrolase glucocerebrosidase. The objective of the present study was to determine whether endolysosomal enzyme activities in cerebrospinal fluid (CSF) differ between PD patients and healthy controls. Activity levels of 6 lysosomal enzymes (β-hexosaminidase, α-fucosidase, β-mannosidase, β-galactosidase, β-glucocerebrosidase, and cathepsin D) and 1 endosomal enzyme (cathepsin E) were measured in CSF from 58 patients with PD (Hoehn and Yahr stages 1-3) and 52 age-matched healthy controls. Enzyme activity levels were normalized against total protein levels. Normalized cathepsin E and β-galactosidase activity levels were significantly higher in PD patients compared with controls, whereas normalized α-fucosidase activity was reduced. Other endolysosomal enzyme activity levels, including β-glucocerebrosidase activity, did not differ significantly between PD patients and controls. A combination of normalized α-fucosidase and β-galactosidase discriminated best between PD patients and controls with sensitivity and specificity values of 63%. In conclusion, the activity of a number of endolysosomal enzymes is changed in CSF from PD patients compared with healthy controls, supporting the alleged role of the endolysosomal pathway in PD pathogenesis. The usefulness of CSF endolysosomal enzyme activity levels as PD biomarkers, either alone or in combination with other markers, remains to be established in future studies. © 2013 Movement Disorder Society.

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