The corpus callosum (CC) is the principal white matter fiber bundle connecting neocortical areas of the two hemispheres. Although an object of extensive research, important details about the anatomical and functional organization of the human CC are still largely unknown. Here we focused on the callosal motor fibers (CMFs) that connect the primary motor cortices (M1) of the two hemispheres. Topography and somatotopy of CMFs were explored by using a combined functional magnetic resonance imaging/diffusion tensor imaging fiber-tracking procedure. CMF microstructure was assessed by fractional anisotropy (FA), and CMF functional connectivity between the hand areas of M1 was measured by interhemispheric inhibition using paired-pulse transcranial magnetic stimulation. CMFs mapped onto the posterior body and isthmus of the CC, with hand CMFs running significantly more anteriorly and ventrally than foot CMFs. FA of the hand CMFs but not FA of the foot CMFs correlated linearly with interhemispheric inhibition between the M1 hand areas. Findings demonstrate that CMFs connecting defined body representations of M1 map onto a circumscribed region in the CC in a somatotopically organized manner. The significant and topographically specific positive correlation between FA and interhemispheric inhibition strongly suggests that microstructure can be directly linked to functional connectivity. This provides a novel way of exploring human brain function that may allow prediction of functional connectivity from variability of microstructure in healthy individuals, and potentially, abnormality of functional connectivity in neurological or psychiatric patients.

Motor learning is important throughout life for acquisition and adjustment of motor skill. The extent of motor learning may be modulated by the history of motor cortex activity, but little is known which metaplasticity rule (homeostatic vs nonhomeostatic) governs this interaction. Here, we explored in nine healthy adults the effects of three different paired associative stimulation (PAS) protocols on subsequent learning of rapid thumb flexion movements. PAS resulted in either a long-term potentiation (LTP)-like increase in excitability of the stimulated motor cortex (PAS LTP ), or a long-term depression (LTD)-like decrease (PAS LTD ), or no change (control condition, PAS CON ). Learning was indexed by the increase in peak acceleration of the trained movement. Delays of 0 and 90 min between PAS and motor practice were tested. At the 0 min delay, PAS LTD strongly facilitated motor learning (homeostatic interaction), and PAS LTP also facilitated learning, although to a lesser extent (nonhomeostatic interaction). At the 90 min delay, PAS LTD facilitated learning, whereas PAS LTP depressed learning (interactions both homeostatic). Therefore, facilitation of learning by previous brain stimulation occurs primarily and most effectively through homeostatic interactions, but at the 0 min delay, nonhomeostatic mechanisms such as LTPinduced blockade of LTD and nonsaturated LTP-induced facilitation of learning might also play a role. The present findings demonstrate that motor learning in humans can be modulated by noninvasive brain stimulation and suggest the possibility of enhancing motor relearning in defined neurological patients.

Frailty results in a 3- to 8-fold increase in risk of postoperative delirium, independent of the EuroSCORE II. "Frail" and "fit" may be considered 2 ends of a continuum, and the risk of postoperative delirium grows as one becomes increasingly frail. The addition of frailty improves the ability of the EuroSCORE II to predict postoperative delirium, pointing to opportunities for improved prevention and management.

Disorders such as borderline personality disorder (BPD) or attention-deficit/hyperactivity disorder (ADHD) are characterized by impulsive behaviors. Impulsivity as used in clinical terms is very broadly defined and entails different categories including personality traits as well as different cognitive functions such as emotion regulation or interference resolution and impulse control. Impulse control as an executive function, however, is neither cognitively nor neurobehaviorally a unitary function. Recent findings from behavioral and cognitive neuroscience studies suggest related but dissociable components of impulse control along functional domains like selective attention, response selection, motivational control, and behavioral inhibition. In addition, behavioral and neural dissociations are seen for proactive vs. reactive inhibitory motor control. The prefrontal cortex with its sub-regions is the central structure in executing these impulse control functions. Based on these concepts of impulse control, neurobehavioral findings of studies in BPD and ADHD were reviewed and systematically compared. Overall, patients with BPD exhibited prefrontal dysfunctions across impulse control components rather in orbitofrontal, dorsomedial, and dorsolateral prefrontal regions, whereas patients with ADHD displayed disturbed activity mainly in ventrolateral and medial prefrontal regions. Prefrontal dysfunctions, however, varied depending on the impulse control component and from disorder to disorder. This suggests a dissociation of impulse control related frontal dysfunctions in BPD and ADHD, although only few studies are hitherto available to assess frontal dysfunctions along different impulse control components in direct comparison of these disorders. Yet, these findings might serve as a hypothesis for the future systematic assessment of impulse control components to understand differences and commonalities of prefrontal cortex dysfunction in impulsive disorders.

In 37 patients with early relapsing-remitting multiple sclerosis (RRMS), a multimodal EP score (mEPS) and clinical scores (Expanded Disability Status Scale (EDSS) and multiple sclerosis functional composite (MSFC)) were obtained prospectively over 24 months. Changes in mEPS correlated with changes in EDSS (Spearman's rho = 0.69, p < 0.0001) and MSFC (rho = -0.41, p < 0.02). Patients with relevant EDSS progression (n = 7) showed stronger mEPS deterioration than clinically stable patients (10.8 +/- 3.2 versus 1.3 +/- 0.8, p < 0.005). Baseline mEPS was not significantly correlated with baseline EDSS but with EDSS after 24 months (rho = 0.39, p < 0.02). The data suggest that serial mEPS measure and moderately predict clinically relevant disease activity in the therapeutically most relevant early stage of RRMS.