Abstract. Transcranial direct current stimulation (tDCS) of the human sensorimotor cortex during physical rehabilitation induces plasticity in the injured brain that improves motor performance. Bi-hemispheric tDCS is a noninvasive technique that modulates cortical activation by delivering weak current through a pair of anodal-cathodal (excitation-suppression) electrodes, placed on the scalp and centered over the primary motor cortex of each hemisphere. To quantify tDCS-induced plasticity during motor performance, sensorimotor cortical activity was mapped during an event-related, wrist flexion task by functional near-infrared spectroscopy (fNIRS) before, during, and after applying both possible bi-hemispheric tDCS montages in eight healthy adults. Additionally, torque applied to a lever device during isometric wrist flexion and surface electromyography measurements of major muscle group activity in both arms were acquired concurrently with fNIRS. This multiparameter approach found that hemispheric suppression contralateral to wrist flexion changed resting-state connectivity from intra-hemispheric to inter-hemispheric and increased flexion speed (p < 0.05). Conversely, exciting this hemisphere increased opposing muscle output resulting in a decrease in speed but an increase in accuracy (p < 0.05 for both). The findings of this work suggest that tDCS with fNIRS and concurrent multimotor measurements can provide insights into how neuroplasticity changes muscle output, which could find future use in guiding motor rehabilitation. © The Authors. Published by SPIE under a Creative Commons Attribution 3.0 Unported License. Distribution or reproduction of this work in whole or in part requires full attribution of the original publication, including its DOI.

In terms of impact on surgeon motion efficiency and operative time under normal surgical conditions, RACC is essentially the same as an expert human driver. However, careful planning and structuring of the surgical suite may yield some small gains in operative time.

Vocal symptoms in spasmodic dysphonia (SD) range from strain-strangle phonation and glottal-stop phonatory breaks of adductor SD to breathy phonation and aspirate phonatory breaks of abductor SD. Many SD subjects show both symptom types. Heterogeneity in vocal symptoms contributes to controversy surrounding the etiology(s) of SD. Acoustic/perceptual analyses of vocal symptoms are inconclusive in resolving this controversy. This investigation moves the search for distinguishing features of adductor and abductor SD to the level of neuromuscular control and analysis of intrinsic laryngeal muscle (adductor and abductor) activity. Subjects rated perceptually as primarily adductor or abductor SD sustained production of vegetative gestures and isolated speech sounds (/i/ and /s/). Qualitative and quantitative analyses of electromyographic signals recorded from thyroarytenoid (TA) failed to differentiate SD subjects by symptom type. Analysis of TA and posterior cricoarytenoid (PCA) activity in one abductor SD revealed high levels in both muscles during production of the voiced vowel. Data suggest that a possible explanation for symptom heterogeneity in SD is the relation between disrupted neuromotor input to laryngeal muscles and reflexive or conscious compensations constrained by laryngeal biomechanics.

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Olanzapine is an "atypical" antipsychotic agent with a high affinity for serotonin 5HT2A/C, 5HT3, 5HT6, and dopamine D1, D2, D3, D4 receptors. Depressed patients with psychotic disorders frequently require treatment with concomitant antipsychotic and antidepressant medications. Imipramine pharmacokinetics serve as a marker for hepatic CYP2D6, CYP1A2, CYP3A activity. An open-label, three-way randomized crossover study was done to determine the safety, pharmacokinetics, and potential for a drug interaction between olanzapine (5 mg) and imipramine (75 mg). Each drug was administered alone and in combination. Nine healthy men, ages 32 to 54 years, enrolled in the study. Psychomotor performance capacities, plasma olanzapine, imipramine, desipramine concentrations, and clinical laboratory tests were measured. Pharmacokinetic variables, vital signs, subjective tests for liveliness, and psychomotor outcomes were analyzed using a two-way ANOVA. Olanzapine was safe. Sedation, postural hypotension, and minor vital sign alterations occurred during all treatments. On the liveliness questionnaire, patients generally reported poorer (less lively) scores with olanzapine alone or coadministered with imipramine versus baseline scores. These effects disappeared within 24 hours after administration. Olanzapine alone and in combination decreased motor-speed tasks (finger tapping and visual-arm random reach) compared with baseline or imipramine treatment. Peak 6-hour changes were statistically significant but clinical importance was only marginal. Olanzapine concentrations were < 19% greater than with imipramine. But olanzapine did not affect the kinetics of imipramine or desipramine and, therefore, did not show a metabolic drug interaction involving CYP2D6.

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