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Defeating neurological obstacles to boost reliable growth immunotherapy.
RESULTS A-tDCS significantly increased CSE as expected at stimulation durations of 22 and 24 min. However, this effect of a-tDCS on CSE decreased and even reversed when stimulation duration increased to 26, 28, and 30 min. Respective alterations of ICF, LIF, and SICI indicate the involvement of glutamatergic, and GABAergic systems in these effects. CONCLUSIONS These results confirm a duration threshold for reversal of the excitability-enhancing effect of a-tDCS with stimulation durations ≥ 26 min. Counter-regulatory mechanisms are discussed as a mechanistic foundation for these effects, which might prevent excessive brain activation. BACKGROUND The function of the primate's posterior parietal cortex (PPC) in sensorimotor transformations is well-established, though in humans its complexity is still challenging. Well-established models indicate that the posterior parietal cortex influences motor output indirectly, by means of connections to the premotor cortex, which in turn is directly connected to the motor cortex. OBJECTIVE The possibility that the PPC could be at the origin of direct afferents to M1 has been suggested in humans but has never been confirmed directly. We aim to do so in the present study by using the novel technique of paired intraoperative cortical stimulation. METHODS In the present cross-sectional study, we assessed during intraoperative monitoring of the corticospinal tract in brain tumour patients the existence of short-latency effects of parietal stimulation on corticospinal excitability to the upper limb. MEPs were evoked by test stimuli over the motor cortex, which were preceded in some trials by conditioning stimuli on the PPC. RESULTS We identified two active cortical loci. One in the inferior parietal lobule exerted short-latency excitatory effects and one in the superior parietal lobule that drove short-latency inhibitory effects on cortical motor output. All active foci were distributed in the rostral portion of the PPC and on the postcentral sulcus. CONCLUSIONS For the first time in humans, the present data show direct evidence in favour of a distributed system of connections from the posterior parietal cortex to the ipsilateral primary motor cortex. In addition, we show that dual cortical stimulation is a novel and efficient technique to investigate intraoperative brain connectivity in the anaesthetized patient. BACKGROUND Recording electroencephalography (EEG) from the targeted cortex immediately before and after focal transcranial electrical stimulation (TES) remains a challenge. METHODS We introduce a hybrid stimulation-recording approach where a single EEG electrode is inserted into the inner electrode of a double-ring montage for focal TES. The new combined electrode was placed at the C3 position of the EEG 10-20 system. Neuronal activity was recorded in two volunteers before and after 20 Hz alternating-current TES at peak-to-peak intensities of 1 and 2 mA. TES-induced electric field distributions were simulated with SIMNIBS software. RESULTS Using the hybrid stimulation-recording set-up, EEG activity was successfully recorded directly before and after TES. Simulations revealed comparable electrical fields in the stimulated cortex for the pseudomonopolar montage with and without embedded EEG electrode. CONCLUSION The hybrid TES-EEG approach can be used to probe after-effects of focal TES on neuronal activity in the targeted cortex. BACKGROUND Neuromodulation by transcranial focused ultrasound (FUS) offers the potential to non-invasively treat specific brain regions, with treatment location verified by magnetic resonance acoustic radiation force imaging (MR-ARFI). OBJECTIVE To investigate the safety of these methods prior to widespread clinical use, we report histologic findings in two large animal models following FUS neuromodulation and MR-ARFI. METHODS Two rhesus macaques and thirteen Dorset sheep were studied. FUS neuromodulation was targeted to the primary visual cortex in rhesus macaques and to subcortical locations, verified by MR-ARFI, in eleven sheep. Both rhesus macaques and five sheep received a single FUS session, whereas six sheep received repeated sessions three to six days apart. The remaining two control sheep did not receive ultrasound but otherwise underwent the same anesthetic and MRI procedures as the eleven experimental sheep. Hematoxylin and eosin-stained sections of brain tissue (harvested zero to eleven days following FUS) were evaluated for tissue damage at FUS and control locations as well as tissue within the path of the FUS beam. TUNEL staining was used to evaluate for the presence of apoptosis in sheep receiving high dose FUS. Entospletinib RESULTS No FUS-related pre-mortem histologic findings were observed in the rhesus macaques or in any of the examined sheep. Extravascular red blood cells (RBCs) were present within the meninges of all sheep, regardless of treatment group. Similarly, small aggregates of perivascular RBCs were rarely noted in non-target regions of neural parenchyma of FUS-treated (8/11) and untreated (2/2) sheep. However, no concurrent histologic abnormalities were observed, consistent with RBC extravasation occurring as post-mortem artifact following brain extraction. Sheep within the high dose FUS group were TUNEL-negative at the targeted site of FUS. CONCLUSIONS The absence of FUS-related histologic findings suggests that the neuromodulation and MR-ARFI protocols evaluated do not cause tissue damage. BACKGROUND Studies have found that pairing vagus nerve stimulation (VNS) with motor activity accelerates cortical reorganization. This synchronous pairing may enhance motor recovery. OBJECTIVE To develop and validate a motor-activated auricular vagus nerve stimulation (MAAVNS) system as a potential neurorehabilitation tool. METHODS We created MAAVNS and validated its function as part of an ongoing clinical trial investigating whether taVNS-paired rehabilitation enhances oromotor learning. We compared 3 different MAAVNS EMG electrode configurations in 3 neonates. The active lead was placed over the buccinator muscle. Reference lead placements were orbital, temporal or frontal. RESULTS The frontal reference lead produced the highest sensitivity (0.87 ± 0.07 (n = 8)) and specificity (0.64 ± 0.13 (n = 8)). Oral sucking reliably triggers MAAVNS stimulation with high confidence. CONCLUSION EMG electrodes placed on target orofacial muscles can effectively trigger taVNS stimuli in infants in a closed loop fashion.
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