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Summers, P. M.

Publications and source records attributed to Summers, P. M..

3 recordsLinked to original sources

Assessing the Intra- and Inter-Subject Reliability of the Perturbational Complexity Index (PCI) of Consciousness for Three Brain Regions Using TMS-EEG

BackgroundThe perturbational complexity index (PCI) is a useful measure of consciousness that combines transcranial magnetic stimulation (TMS) with electroencephalography (EEG). However, the PCI has not been assessed for reliability between sessions nor is there a clear best stimulation target to acquire a PCI. Objective/HypothesisWe assessed the reliability of within-subject PCIs between 3 sessions with stimulation over the same premotor, motor, and parietal targets between visits, hypothesizing that we could determine a most reliable TMS-EEG target to acquire PCIs in healthy, conscious adults. MethodsPCIs were acquired for 9 participants (5 women) over 3 sessions within a week. A 64 channel EEG system was used with all electrode impedances [&le;] 10k{Omega}. Premotor, motor, and parietal stimulation targets were identified using a real-time Matlab graphical user interface (GUI). Neuronavigation using an MRI-template brain ensured that every TMS pulse was delivered within 3.0mm and 5{degrees} of the stimulation target. ResultsPremotor, motor, and parietal PCIs all had significant PCIs (all p < 0.05). However, parietal and motor PCIs had excellent reliability (ICCs = 0.927 and 0.857 respectively) whereas premotor PCIs had good reliability (ICC = 0.737). PCIs were similar between brain sites within each subject in a single visit, but with only a moderate effect (p = 0.024, ICC = 0.480). PCIs on a group level did not differ between brain sites (p = 0.589). ConclusionsThe PCI is a reliable measure over this timeframe within each subject for single brain targets. PCIs for parietal and motor sites are most similar between visits. Due to only moderate similarity between PCIs from three brain sites within each session, PCIs should be acquired over at least two brain sites, with parietal and motor regions as the top candidates.

neuroscience↗

Transcranial Electrical Stimulation Motor Threshold Combined with Reverse-Calculated Electric Field Modeling Can Determine Individualized tDCS Dosage

BackgroundUnique amongst brain stimulation tools, transcranial direct current stimulation (tDCS) currently lacks an easy method for individualizing dosage.\n\nObjectiveCan one individually dose tDCS? We developed a novel method of reverse-calculating electric-field (E-field) models based on Magnetic Resonance Imaging (MRI) scans that can determine individualized tDCS dose. We also sought to develop an MRI-free method of individualizing tDCS dose by measuring transcranial magnetic stimulation (TMS) motor threshold (MT) and single pulse, suprathreshold transcranial electrical stimulation (TES) MT and regressing it against E-field modeling.\n\nMethodsIn 29 healthy adults, we acquired TMS MT, TES MT, and structural MRI scans with a fiducial marking the motor hotspot. We then computed a \"reverse-calculated tDCS dose\" of tDCS applied at the scalp needed to cause a 1.00V/m E-field at the cortex. Finally, we examined whether the predicted E-field values correlated with each participants measured TMS MT or TES MT.\n\nResultsWe were able to determine a reverse-calculated tDCS dose for each participant. The Transcranial Electrical Stimulation MT, but not the Transcranial Magnetic Stimulation MT, significantly correlated with the calculated tDCS dose determined by E-field modeling (R2 = 0.509, p < 0.001).\n\nConclusionsReverse-calculation E-field modeling, alone or in combination with TES MT, shows promise as a method to individualize tDCS dose. The large range of the reverse-calculated tDCS doses between subjects underscores the likely need to individualize tDCS dose. If these results are confirmed in future studies, TES MT may evolve into an inexpensive and quick method to individualize tDCS dose.

neuroscience↗

In Vivo Two-Photon Imaging of Neuronal and Vascular Responses in Mice Chronically Exposed to Ethanol

The effects of ethanol on brain function have been extensively studied using a variety of in vitro and in vivo techniques. For example, electrophysiological studies using brain slices from rodents and nonhuman primates have demonstrated that acute and chronic exposure to ethanol alters the intrinsic excitability and synaptic signaling of neurons within cortical and sub-cortical areas of the brain. In humans, neuroimaging studies reveal alterations in measures of brain activation and connectivity in subjects with alcohol use disorders. While complementary, these methods are inherently limited due to issues related to either disruption of normal sensory input (in vitro slice studies) or resolution (whole brain imaging). In the present study, we used 2-photon laser scanning microscopy in intact animals to assess the impact of chronic ethanol exposure on sensory evoked neuronal and vascular responses. Adult male C57BL/6J mice were exposed to 4 weekly cycles of chronic intermittent ethanol (CIE) exposure while control mice were exposed to air. After withdrawal ([&le;] 72 hr), a cranial window was placed over the primary visual cortex (V1) and sensory evoked responses were monitored using the calcium indicator OGB-1. CIE exposure produced small but significant changes in response amplitude (decrease) and orientation selectivity of V1 neurons (increase). While arteriole diameter did not differ between control and CIE mice under baseline conditions, sensory-evoked dilation was enhanced in vessels from CIE exposed mice as compared to controls. This was accompanied by a reduced latency in response to stimulation. In separate experiments, pial arteriole diameter was measured in the barrel cortex of control and CIE exposed mice. Baseline diameter of barrel cortex arterioles was similar between control and CIE exposed mice but unlike vessels in V1, sensory-evoked dilation of barrel cortex arterioles was similar between the two groups. Together the results of these studies suggest that chronic exposure to alcohol induces changes in neurovascular coupling that are region dependent.

neuroscience↗