How salience enhances inhibitory control: An analysis of electro-cortical mechanisms

Stop-signal tasks (SSTs) combined with human electro-cortical recordings (Event-Related Potentials, ERPs) have revealed mechanisms associated with successful stopping (relative to failed), presumably contributing to inhibitory control. The corresponding ERP signatures have been labeled stop N1 (+/- 100-ms latency), stop N2 (200 ms), and stop P3 (160-250 ms), and argued to reflect more proactive (N1) versus more reactive (N2, P3) mechanisms. However, stop N1 and stop N2, as well as latencies of stop-P3, appear to be quite inconsistent across studies. The present work addressed the possible influence of stop-signal salience, expecting high salience to induce clear stop N1s but reduced stop N2s, and short-latency stop P3s. Three SST varieties were combined with high-resolution EEG. An imperative visual (go) stimulus was occasionally followed by a subsequent (stop) stimulus that signalled to withhold the just initiated response. Stop-Signal Reaction Times (SSRTs) decreased linearly from visual-low to visual-high-salience to auditory. Auditory Stop N1 was replicated. A C1-like visual evoked potential (latency < 100 ms) was observed only with high salience, but not robustly associated with successful versus failed stops. Using the successful-failed contrast a visual stop-N1 analogue (112-156 ms post-stop-signal) was identified, as was right-frontal stop N2, but neither was sensitive to salience. Stop P3 had shorter latency for high than for low salience, and the extent of the early high-salience stop P3 correlated inversely with SSRT. These results suggest that salience-enhanced inhibitory control as manifest in SSRTs is associated with reactive rather than proactive electrocortical mechanisms.

Neural correlates of integration processes during dynamic face perception

Integrating the spatiotemporal information acquired from the highly dynamic world around us is essential to navigate, reason, and decide properly. Although this is particularly important in a face-to-face conversation, very little research to date has specifically examined the neural correlates of temporal integration in dynamic face perception. Here we present statistically robust observations regarding the brain activations measured via electroencephalography (EEG) that are specific to the temporal integration. To that end, we generate videos of neutral faces of individuals and non-face objects, modulate the contrast of the even and odd frames at two specific frequencies ($$f_1$$ f 1 and $$f_2$$ f 2 ) in an interlaced manner, and measure the steady-state visual evoked potential as participants view the videos. Then, we analyze the intermodulation components (IMs: ($$nf_1\pm mf_2$$ n f 1 ± m f 2 ), a linear combination of the fundamentals with integer multipliers) that consequently reflect the nonlinear processing and indicate temporal integration by design. We show that electrodes around the medial temporal, inferior, and medial frontal areas respond strongly and selectively when viewing dynamic faces, which manifests the essential processes underlying our ability to perceive and understand our social world. The generation of IMs is only possible if even and odd frames are processed in succession and integrated temporally, therefore, the strong IMs in our frequency spectrum analysis show that the time between frames (1/60 s) is sufficient for temporal integration.

Simultaneous measurement of intra-epidermal electric detection thresholds and evoked potentials for observation of nociceptive processing following sleep deprivation

Sleep deprivation has been shown to increase pain intensity and decrease pain thresholds in healthy subjects. In chronic pain patients, sleep impairment often worsens the perceived pain intensity. This increased pain perception is the result of altered nociceptive processing. We recently developed a method to quantify and monitor altered nociceptive processing by simultaneous tracking of psychophysical detection thresholds and recording of evoked cortical potentials during intra-epidermal electric stimulation. In this study, we assessed the sensitivity of nociceptive detection thresholds and evoked potentials to altered nociceptive processing after sleep deprivation in an exploratory study with 24 healthy male and 24 healthy female subjects. In each subject, we tracked nociceptive detection thresholds and recorded central evoked potentials in response to 180 single- and 180 double-pulse intra-epidermal electric stimuli. Results showed that the detection thresholds for single- and double-pulse stimuli and the average central evoked potential for single-pulse stimuli were significantly decreased after sleep deprivation. When analyzed separated by sex, these effects were only significant in the male population. Multivariate analysis showed that the decrease of central evoked potential was associated with a decrease of task-related evoked activity. Measurement repetition led to a decrease of the detection threshold to double-pulse stimuli in the mixed and the female population, but did not significantly affect any other outcome measures. These results suggest that simultaneous tracking of psychophysical detection thresholds and evoked potentials is a useful method to observe altered nociceptive processing after sleep deprivation, but is also sensitive to sex differences and measurement repetition.

Standardization and Validation of the Flash Visual Evoked Potential-P2 Conversion Scores in the Diagnosis of Amnestic Mild Cognitive Impairment and Alzheimer's Dementia

Amnestic mild cognitive impairment (aMCI), which is characterized by normal daily activity, but a significant decline in episodic memory, is now widely accepted as a risk factor for the development of Alzheimer's dementia (AD). Research suggests that many of the same neuropathological changes associated with AD also occur in patients diagnosed with aMCI. A recent review of the literature revealed that the latency of the flash visual-evoked potential-P2 (FVEP-P2) may possess pathognomonic information that may assist in the early detection of aMCI. While standards exist for the recording of FVEP-P2, individual clinics often use recording parameters that may differ, resulting in latencies that may not generalize beyond the clinic that produced them. The present article illustrates the process by which the FVEP-P2 latency can be standardized across clinics using FVEP-P2 Conversion Scores. We then demonstrate the diagnostic accuracy of the newly developed scores. Method: In the present investigation, we used the previously unpublished data containing the FVEP-P2 latencies of 45 AD and 60 controls. Result: We were able to demonstrate the process by which individual clinics may first standardize FVEP-P2 latencies and then examine patient performance using FVEP-P2 Conversion Scores, providing clinicians with a richer context from which to examine the patient performance. Conclusion: Consistent with the findings of previous research, the findings of the present investigation support the use of the FVEP-P2 Conversion Scores in the diagnosis of AD. Future directions, including the modification of recording parameters associated with the FVEP-P2, are also discussed.

Prevention of trigeminocardiac reflex-induced severe bradycardia during cerebral aneurysm clipping surgery by topical anesthesia of the dura surface and atropine administration: a case report

Background Trigeminocardiac reflex (TCR) by stimulation of the sensory branch of the trigeminal nerve induces transient bradycardia and hypotension. We report a case in which light mechanical stimulation to the dura mater during brain surgery induced severe bradycardia. Case presentation A 77-year-old woman with bradycardia-tachycardia syndrome was scheduled for clipping of an unruptured left middle cerebral artery aneurysm. General anesthesia was performed with propofol, remifentanil, and rocuronium. Before starting surgery, the function of the pyramidal tract was examined by motor evoked potential. Transcranial electric stimulation for motor evoked potential induced atrial fibrillation and tachycardia. Continuous administration of landiolol was started and verapamil was used for tachycardia. During detachment of the dura mater from the bone, an electrocardiogram suddenly showed sinus arrest for 6 s. Immediately after the manipulation was interrupted, a junctional rhythm appeared. However, light touch to the dura mater induced severe bradycardia again, and atropine was therefore administered. In addition, the dura surface was anesthetized with topical lidocaine infiltration. After that, light touch-induced bradycardia was prevented. Conclusions We experienced a case of severe bradycardia during surgery due to TCR caused by light mechanical stimulation to the dura mater. Topical anesthesia of the dura surface and atropine administration were effective for preventing TCR-induced bradycardia.