• Neuroinformatics
• 2014-2023close

Abstract Objective. The power spectrum of the human electroencephalogram (EEG) as a function of frequency is a mix of brain oscillations (Osc) (e.g. alpha activity around 10 Hz) and non-Osc or noise of uncertain origin. ‘White noise’ is uniformly distributed over frequency, while ‘pink noise’ has an inverse power-frequency relation (power ∝ 1/f). Interest in EEG pink noise has been growing, but previous human estimates appear methodologically flawed. We propose a new approach to extract separate valid estimates of pink and white noise from an EEG power spectrum. Approach. We use simulated data to demonstrate its effectiveness compared with established procedures, and provide an illustrative example from a new resting eyes-open (EO) and eyes-closed (EC) dataset. The topographic characteristics of the obtained pink and white noise estimates are examined, as is the alpha power in this sample. Main results. Valid pink and white noise estimates were successfully obtained for each of our 5400 individual spectra (60 participants × 30 electrodes × 3 conditions/blocks [EO1, EC, EO2]). The 1/f noise had a distinct central scalp topography, and white noise was occipital in distribution, both differing from the parietal topography of the alpha Osc. These differences point to their separate neural origins. EC pink and white noise powers were globally greater than in EO. Significance. This valid estimation of pink and white noise in the human EEG holds promise for more accurate assessment of oscillatory neural activity in both typical and clinical groups, such as those with attention deficits. Further, outside the human EEG, the new methodology can be generalized to remove noise from spectra in many fields of science and technology.

Selective attention has traditionally been viewed as a sensory processing modulator that promotes cognitive processing efficiency by favoring relevant stimuli while inhibiting irrelevant stimuli. However, the cross-modal processing of irrelevant information during working memory (WM) has been rarely investigated. In this study, the modulation of irrelevant auditory information by the brain during a visual WM task was investigated. The N100 auditory evoked potential (N100-AEP) following an auditory click was used to evaluate the selective attention to auditory stimulus during WM processing and at rest. N100-AEP amplitudes were found to be significantly affected in the left-prefrontal, mid-prefrontal, right-prefrontal, left-frontal, and mid-frontal regions while performing a high WM load task. In contrast, no significant differences were found between N100-AEP amplitudes in WM states and rest states under a low WM load task in all recorded brain regions. Furthermore, no differences were found between the time latencies of N100-AEP troughs in WM states and rest states while performing either the high or low WM load task. These findings suggested that the prefrontal cortex (PFC) may integrate information from different sensory channels to protect perceptual integrity during cognitive processing.

AbstractBOLD fMRI is widely applied in human neuroscience but is limited in its spatial specificity due to a cortical‐depth‐dependent venous bias. This reduces its localization specificity with respect to neuronal responses, a disadvantage for neuroscientific research. Here, we modified a submillimeter BOLD protocol to selectively reduce venous and tissue signal and increase cerebral blood volume weighting through a pulsed saturation scheme (dubbed Arterial Blood Contrast) at 7 T. Adding Arterial Blood Contrast on top of the existing BOLD contrast modulated the intracortical contrast. Isolating the Arterial Blood Contrast showed a response free of pial‐surface bias. The results suggest that Arterial Blood Contrast can modulate the typical fMRI spatial specificity, with important applications in in‐vivo neuroscience.

Bright-light interventions have successfully been used to reduce depression symptoms in patients with seasonal affective disorder, a depressive disorder most frequently occurring during seasons with reduced daylight availability. Yet, little is known about how light exposure impacts human brain function, for instance on risk taking, a process affected in depressive disorders. Here we examined the modulatory effects of bright-light exposure on brain activity during a risk-taking task. Thirty-two healthy male volunteers living in the greater Copenhagen area received 3weeks of bright-light intervention during the winter season. Adopting a double-blinded dose-response design, bright-light was applied for 30minutes continuously every morning. The individual dose varied between 100 and 11.000lx. Whole-brain functional MRI was performed before and after bright-light intervention to probe how the intervention modifies risk-taking related neural activity during a two-choice gambling task. We also assessed whether inter-individual differences in the serotonin transporter-linked polymorphic region (5-HTTLPR) genotype influenced the effects of bright-light intervention on risk processing. Bright-light intervention led to a dose-dependent increase in risk-taking in the LA/LA group relative to the non-LA/LA group. Further, bright-light intervention enhanced risk-related activity in ventral striatum and head of caudate nucleus in proportion with the individual bright-light dose. The augmentation effect of light exposure on striatal risk processing was not influenced by the 5-HTTLPR-genotype. This study provides novel evidence that in healthy non-depressive individuals bright-light intervention increases striatal processing to risk in a dose-dependent fashion. The findings provide converging evidence that risk processing is sensitive to bright-light exposure during winter.

Abstract Background Fine motor and coordination problems are frequently reported among adolescents born preterm. We aimed to assess performance in hand coordination tasks and to compare concurrent brain activation between adolescents born very preterm and at term at 13 years. Methods A total of 34 right-handed adolescents born very preterm (gestational age less than 32 weeks/birth weight ≤1500 grams) and 37 controls born at term during 2003 to 2006 in Turku University Hospital, Finland, were recruited. At 13 years, finger opposition and diadochokinesis were assessed, and brain functional magnetic resonance imaging data were acquired while the adolescents performed unimanual hand coordination tasks in response to visual cue. Results Adolescents born very preterm performed similar to controls in hand coordination tasks. The very preterm group evoked greater brain activation than the controls in the right precentral gyrus and in the right postcentral gyrus during left-hand finger opposition and in the right postcentral gyrus during left-hand diadochokinesis. Within the very preterm group, lower gestational age was associated with reduced activation in the left superior parietal lobule during right-hand diadochokinesis. Regarding left-hand tasks, lower gestational age was associated with stronger activation in the right cerebellar lobule V and left cerebellar lobule VI during finger opposition and stronger activation in the right superior parietal lobule during diadochokinesis. Conclusions Very preterm birth affected hand coordination-related brain activation. Most of the effects were found for nondominant hand. Clinical performance during the hand coordination tasks was similar in adolescents born very preterm and controls.

Creutzfeldt-Jakob disease (CJD) is a fatal disease caused by the accumulation of abnormal prion proteins in neurological tissues. Routine notification data reveal that NSW has similar rates of CJD to other states and territories in Australia; however, it is likely that there is significant under-ascertainment of cases. It is important that clinicians and public health staff remain vigilant for the clinical signs of CJD and understand the limitations of the different diagnostic tests available. This paper provides a brief overview of the epidemiology of CJD in NSW, as well as current issues in the diagnosis and public health investigation of CJD.

Previous studies have shown a close relationship between the serotonin system and working memory (WM), but the neural mechanism for the role of the serotonin system on the WM is unclear. The frontoparietal network is involved in WM and is associated with the serotonin system. Therefore, this study investigated the interaction effect of the serotonin transporter-linked polymorphic region (5-HTTLPR) and the polymorphism in the serotonin 1A receptor gene (rs6295) on the frontoparietal network obtained from the independent component analysis in a large, young Chinese sample population. The current study found a significant interaction effect of 5-HTTLPR and rs6295 on the connectivity within the right frontoparietal network, specifically in the middle frontal gyrus and inferior parietal lobule. Moreover, the mean connectivity in the right inferior parietal lobule was positively correlated with WM performance. These brain network analysis findings could provide a new perspective on the neural mechanisms of gene-gene interactions and on individual differences in cognitive functions.

AbstractRecent evidence has shown the presence of a “rich club” in the brain, which constitutes a core network of highly interconnected and spatially distributed brain regions, important for high‐order cognitive processes. This study aimed to map the rich club organization in 17 young patients with moderate to severe TBI (15.71 ± 1.75 years) in the chronic stage of recovery and 17 age‐ and gender‐matched controls. Probabilistic tractography was performed on diffusion weighted imaging data to construct the edges of the structural connectomes using number of streamlines as edge weight. In addition, the whole‐brain network was divided into a rich club network, a local network and a feeder network connecting the latter two. Functional outcome was measured with a parent questionnaire for executive functioning. Our results revealed a significantly decreased rich club organization (p values < .05) and impaired executive functioning (p < .001) in young patients with TBI compared with controls. Specifically, we observed reduced density values in all three subnetworks (p values < .005) and a reduced mean strength in the rich club network (p = .013) together with an increased mean strength in the local network (p = .002) in patients with TBI. This study provides new insights into the nature of TBI‐induced brain network alterations and supports the hypothesis that the local subnetwork tries to compensate for the biologically costly subnetwork of rich club nodes after TBI.