The Neural Markers of Self-Caught and Probe-Caught Mind Wandering: An ERP Study

Mind-wandering (MW) is a common phenomenon, defined as task-unrelated thoughts. This study is based on event-related potentials (ERPs), using modified sustained attention to response task (modified SART, mSART) to discuss the neural patterns of different types of MW. In the current study, we defined the MW realized by participants as self-caught MW, and the MW measurement acquired by probes as probe-caught MW. The behavioral results showed that the reaction times (RTs) during self-caught MW were greater than those during non-self-caught MW. The ERP results showed that during self-caught MW, the mean amplitudes of N1 decreased significantly, indicating that the participants’ attention had deviated from the current task. The increase in the mean amplitudes of P2 during self-caught MW indicated lower vigilance. We also found that the mean amplitudes of N300 reduced during self-caught MW, which indicated that cognitive control or monitoring might be affected by self-caught MW. The average amplitudes of P300 were significantly lower during probe-caught MW than during on-task, indicating the impact on high-level cognitive processing. In addition, the amplitudes of N1, P2, and N300 in anterior regions were greater than those in posterior regions. P300 amplitudes during probe-caught MW in the right hemisphere were greater than those of the left hemisphere. In summary, our research results demonstrated that alertness and cognitive processing decreased during both self-caught MW and probe-caught MW. ERPs were statistically different under the conditions of self-caught MW and probe-caught MW. The current study provided new insights into the relationship between MW and neural markers. It was the first study exploring the ERP correlates between self-caught MW and probe-caught MW based on mSART.

First Language Attrition: What It Is, What It Isn’t, and What It Can Be

This review aims at clarifying the concept of first language attrition by tracing its limits, identifying its phenomenological and contextual constraints, discussing controversies associated with its definition, and suggesting potential directions for future research. We start by reviewing different definitions of attrition as well as associated inconsistencies. We then discuss the underlying mechanisms of first language attrition and review available evidence supporting different background hypotheses. Finally, we attempt to provide the groundwork to build a unified theoretical framework allowing for generalizable results. To this end, we suggest the deployment of a rigorous neuroscientific approach, in search of neural markers of first language attrition in different linguistic domains, putting forward hypothetical experimental ways to identify attrition’s neural traces and formulating predictions for each of the proposed experimental paradigms.

DOES FEAR OF MOVEMENT ALTER BRAIN ACTIVITY? INVESTIGATING THE NEURAL MARKERS OF KINESIOPHOBIA IN PEDIATRIC PATIENTS WITH PATELLOFEMORAL PAIN

Background: Patellofemoral pain (PFP) is a chronic knee condition that inhibits movement quality and can cascade into kinesiophobia (i.e., fear of pain/movement). Despite its high prevalence in adolescent girls, PFP etiology has remained elusive, potentially due to an incomplete understanding of how pain, motor control, and kinesiophobia interact with central nervous system (CNS) functioning. Discovering linkages between motor control, kinesiophobia, and the CNS for patients with PFP could provide novel opportunities to refine neural therapeutic strategies for enhanced, personalized treatment approaches. Hypothesis/Purpose: To identify neural markers of kinesiophobia in pediatric patients with PFP. Methods: Adolescent girls clinically diagnosed with PFP ( n = 14; 14.3 ± 3.2 yrs) were positioned supine in a magnetic resonance imaging (MRI) scanner. A modified Clarke’s test (patellofemoral grind test) was administered to the left knee of patients during brain functional MRI (fMRI) acquisition. The experimenter placed a hand at the superior patellar border applying intermittent distal pressure while the patient contracted her quadriceps. Patients also completed a quadriceps contraction test without application of external pressure (control). Kinesiophobia was measured using the Tampa Scale of Kinesiophobia. fMRI analyses compared brain activation between the two tasks, and correlation analyses were performed to assess relationships between task-induced brain activity and kinesiophobia. Statistical corrections were made to account for multiple, voxel-wise comparisons. Results: Evidenced in Table 1 and Figure 1A, neuroimaging analyses revealed distinct bidirectional activation during the Clarke’s test compared to the control (all p corrected < .05, all z max > 3.1). Table 1 and Figure 1B further highlight that greater kinesiophobia was associated with increased brain activity during the Clarke’s test in two clusters (both p corrected < .05, both z max > 3.1), but no relationships between kinesiophobia and brain activity during the control test were observed (all p corrected > .05, all z max < 3.1). Conclusion: The current results indicate that the Clarke’s test induced differential pain-related brain activity relative to the control (e.g., paracingulate gyrus). The patients’ degree of kinesiophobia was also related to brain activity in regions important for sensorimotor control, attention, and pain. Collectively, these data indicate that PFP may be due to alterations in nociceptive processing throughout the CNS, providing novel complementary pathways for targeted restoration of patellofemoral joint dysfunction. Future research should consider combined mechanistic pain profiling, sensorimotor, psychometric, and CNS assessments to identify patients most susceptible to kinesiophobia to refine treatment approaches that work towards a goal of disease prevention. Tables/Figures: [Figure: see text][Table: see text]

Prognostic Structural Neural Markers of MRI in Response to Mechanical Thrombectomy for Basilar Artery Occlusion

Objective: Mechanical thrombectomy (MT) has been an effective first-line therapeutic strategy for ischemic stroke. With impairment characteristics separating it from anterior circulation stroke, we aimed to explore prognostic structural neural markers for basilar artery occlusion (BAO) after MT.Methods: Fifty-four BAO patients with multi-modal magnetic resonance imaging at admission from the multicenter real-world designed BASILAR research were enrolled in this study. Features including volumes for cortical structures and subcortical regions, locations and volumes of infarctions, and white matter hyperintensity (WMH) volumes were recorded from all individuals. The impact features were identified using ANCOVA and logistic analysis. Another cohort (n = 21) was further recruited to verify the prognostic roles of screened prognostic structures.Results: For the primary clinical outcome, decreased brainstem volume and total infarction volumes from mesencephalon and midbrain were significantly related to reduced 90-day modified Rankin score (mRS) after MT treatment. WMH volume, WMH grade, average cortex thickness, white matter volume, and gray matter volume did not exhibit a remarkable relationship with the prognosis of BAO. The increased left caudate volume was obviously associated with early symptomatic recovery after MT. The prognostic role of the ratio of pons and midbrain infarct volume in brainstem was further confirmed in another cohort with area under the curve (AUC) = 0.77.Conclusions: This study was the first to provide comprehensive structural markers for the prognostic evaluation of BAO. The fully automatic and semiautomatic segmentation approaches in our study supported that the proportion of mesencephalon and midbrain infarct volume in brainstem was a crucial prognostic structural neural marker for BAO.