Front Hum Neurosci
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The sensitizing effect of capsaicin has been previously characterized using laser and contact heat evoked potentials (LEPs and CHEPs) by stimulating in the primary area of hyperalgesia. Interestingly, only CHEPs reveal changes consistent with notion of peripheral sensitization (i.e., reduced latencies). The aim of this study was to investigate contact heat stimulation parameters necessary to detect peripheral sensitization related to the topical application of capsaicin, and therefore significantly improve the current method of measuring peripheral sensitization via CHEPs. ⋯ These findings suggest that earlier recruitment of capsaicin-sensitized afferents occurs between 35 and 42°C, as stimulations from 42°C baseline were unchanged by capsaicin. This is in line with reduced thresholds of type II A-delta mechanoheat (AMH) nociceptors following sensitization. Conventional CHEP stimulation, with a baseline temperature below 42°C, is well suited to objectively detect evidence of peripheral sensitization.
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Background: Major depressive disorder (MDD) and fibromyalgia (FM) present overlapped symptoms. Although the connection between these two disorders has not been elucidated yet, the disruption of neuroplastic processes that mediate the equilibrium in the inhibitory systems stands out as a possible mechanism. Thus, the purpose of this cross-sectional exploratory study was: (i) to compare the motor cortex inhibition indexed by transcranial magnetic stimulation (TMS) measures [short intracortical inhibition (SICI) and intracortical facilitation (ICF)], as well as the function of descending pain modulatory systems (DPMS) among FM, MDD, and healthy subjects (HS); (ii) to compare SICI, ICF, and the role of DPMS evaluated by the change on Numerical Pain Scale (NPS) during the conditioned pain modulation test (CPM-test) between FM and MDD considering the BDNF-adjusted index; (iii) to assess the relationship between the role of DPMS and the BDNF-adjusted index, despite clinical diagnosis. ⋯ The BDNF-adjusted index was positively correlated with the disinhibition of the DPMS. Conclusion: These findings support the hypothesis that in FM a deteriorated function of cortical inhibition, indexed by a higher SICI parameter, a lower function of the DPMS, together with a higher level of BDNF indicate that FM has different pathological substrates from depression. They suggest that an up-regulation phenomenon of intracortical inhibitory networks associated with a disruption of the DPMS function occurs in FM.
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Auricular vagal nerve stimulation (AVNS) is an evolving neuromodulation technology that has a wide range of therapeutic applications across multiple disciplines of medical science. To date, AVNS results had been interpreted in the context of a monolog concept of the auricular branch of the vagus nerve (ABVN): that this is the sole network of the mechanism of action and/or structure in the auricular area of the stimulation in the context of activations in the brainstem nuclei, including the nucleus tractus solitarius (NTS), locus coeruleus (LC), trigeminal brainstem nuclei, and the nucleus cuneatus. ⋯ In addition, the unique cortical representation of the human ear and interspecies differences in the auricula are discussed. The detailed auricular anatomy of the AVNS zone explored in the present study references structural and functional neural network information to overcome default designs and misinterpretations of existing research on AVNS to provide a better foundation for future investigations that use this modality.
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A recent multicenter trial provided Class I evidence that for patients with an episodic migraine, non-invasive vagus nerve stimulation (nVNS) significantly increases the probability of having mild pain or being pain-free 2 h post-stimulation. Here we aimed to investigate the potential effect of nVNS in the modulation of spontaneous and pain related bioelectrical activity in a subgroup of migraine patients enrolled in the PRESTO trial by using resting-state electroencephalography and trigeminal laser-evoked potentials (LEPs). LEPs were recorded for 27 migraine patients who received active or sham nVNS over the cervical vagus nerve. ⋯ The sham device also attenuated the P2 amplitude evoked by the left trigeminal branch at T1 and T2, but this attenuation did not reach significance. No changes were observed for N1 amplitude, N1, N2, P2 latency, or pain rating. nVNS induced an increase of EEG power in both slow and fast rhythms, but this effect was not significant as compared to the sham device. These findings suggest that nVNS acts on the cortical areas that are responsible for trigeminal pain control and pave the ground for future studies aimed at confirming the possible correlations with clinical outcomes, including the effect on symptoms that are directly correlated with trigeminal pain processing and modulation.
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The neural networks that constitute corticostriatothalamocortical circuits between prefrontal cortex and subcortical structure provide a heuristic framework for bridging gaps between neurocircuitry and executive dysfunction in attention deficit hyperactivity disorder (ADHD). "Cool" and "Hot" executive functional theory and the models of dual pathway are supposed to be applied within the neuropsychology of ADHD. The theoretical model elaborated response inhibition and delayed gratification in ADHD. We aimed to review and summarize the literature about the circuits on ADHD and ADHD-related comorbidities, as well as the effects of neurocircuitry on the executive dysfunction in ADHD.