Oscillatory cortical activities in the gamma band in the human EEG induced by visual stimuli--representation of the stimulus?

The present work presents three experiments investigating cortical activities in the gamma band in humans. On the basis of theoretical models and animal experiments, synchronized oscillatory neuronal activity is discussed as the key mechanism by which the brain binds information processesed in different cortical areas to form a percept. Using an identical stimulation design--the same as used in animal studies--it was shown that induced gamma band responses in the EEG resemble the same features as those found in the intracortical recordings of animals. In addition, the present work demonstrates that these cortical activities are not higher harmonics of the alpha band and that they are sensitive to the features of the stimulus. These results support the notion that gamma band activity is not just a by-product of neuronal activity and that alpha- and gamma band activities most certainly represent different cortical functional states.     

Are event-related potential components generated by phase resetting of brain oscillations? A critical discussion

The event-related potential (ERP) is one of the most popular measures in human cognitive neuroscience. During the last few years there has been a debate about the neural fundamentals of ERPs. Two models have been proposed: The evoked model states that additive evoked responses which are completely independent of ongoing background electroencephalogram generate the ERP. On the other hand the phase reset model suggests a resetting of ongoing brain oscillations to be the neural generator of ERPs. Here, evidence for either of the two models is presented and validated, and their possible impact on cognitive neuroscience is discussed. In addition, future prospects on this field of research are presented.     

Can I have a quick word? Early electrophysiological manifestations of psycholinguistic processes revealed by event-related regression analysis of the EEG

We applied multiple linear regression analysis to event-related electrophysiological responses to words and pseudowords in a visual lexical decision task, yielding event-related regression coefficients (ERRCs) instead of the traditional event-related potential (ERP) measure. Our main goal was to disentangle the earliest ERP effects of the length of letter strings ("word length") and orthographic neighbourhood size (Coltheart's "N"). With respect to N, existing evidence is still ambiguous with respect to whether effects of N reflect early access to lexico-semantic information, or whether they occur at later decision or verification stages. In the present study, we found distinct neurophysiological manifestations of both N and word length around 100ms after word onset. Importantly, the effect of N distinguished between words and pseudowords, while the effect of word length did not. Minimum norm source estimation revealed the most dominant sources for word length in bilateral posterior brain areas for both words and pseudowords. For N, these sources were more left-lateralised and consistent with perisylvian brain areas, with activation peaks in temporal areas being more anterior for words compared to pseudowords. Our results support evidence for an effect of N at early and elementary stages of word recognition. We discuss the implications of these results for the time line of word recognition processes, and emphasise the value of ERRCs in combination with source analysis in psycholinguistic and cognitive brain research.     

Are lipid peroxidation processes induced by changes in the cell wall structure and how are these processes connected with diseases?

Apparently nature uses the unique sensitivity of polyunsaturated fatty acids (PUFAs) versus oxygen to generate chemical signals if the surface of a cell is influenced by an outside or inside event; for instance the attack of microorganisms, proliferation, aging or by treatment of isolated cells with surfactants. It seems that mammalian and plant cells respond equally to such changes in their structures by transformation of polyunsaturated fatty acids localized in the phospholipid layer of the cell wall to lipidhydroperoxides (LOOHs). These lipid peroxidation (LPO) processes involve all PUFAs, not only arachidonic acid.Slight physiological changes of the cell wall for instance by proliferation seem to activate enzymes, e.g., phospholipases and lipoxygenases (LOX). When an outside impact (for instance by attack of microorganisms) exceeds a certain level LOX commit suicide and liberate iron ions. These start a nonenzymatic LPO. Enzymatic and nonenzymatic LPO distinguish fundamentally which has not been recognized in the past. In the enzymatic LPO processes peroxyl radicals generated as intermediates cannot leave the enzyme complex. In contrast in a nonenzymatic LPO process peroxyl radicals are not trapped. They attack nearly any kind of biological molecules, for instance proteins. Thus only the amount of an outside impact decides if proliferation, apoptosis, or necrosis is started.Some evidence indicates that cancer might be the consequence of a low response of cells to induce apoptotic LPO processes. In contrast to high level of LPO processes induces diseases combined with inflammation, for instance rheumatic arthritis. After consumption of food rich in linoleic acid its LPO products become increased in low density lipoprotein (LDL). This LDL is able to enter endothelial cells and damage cells from inside, long before an inflammatory response is detectable.     

How much does phase resetting contribute to event-related EEG abnormalities in schizophrenia?

Objective: Patients suffering from schizophrenia demonstrate impaired low frequency electrophysiological responses to stimuli, but it remains unclear whether these abnormalities arise from phase resetting of ongoing oscillations, new phase-locked (evoked) activity or non-phase-locked (induced) activity. Our goal is to clarify the contribution of each of these three processes to the impairment of neural activity during information processing in schizophrenia, by using statistics that do not confound increases in the mean post-stimulus signal with phase resetting. Methods: Thirty-four male schizophrenia patients and 34 healthy matched controls performed an auditory oddball task. We applied the analysis procedure developed by Martinez-Montes et al. [18] based on complex-valued wavelet transform to event-related signal elicited by target stimuli. Results: The largest abnormalities were found for phase-locked delta (1–4 Hz) and non-phase-locked theta (4–8 Hz). Delta phase resetting was moderately impaired and related to symptoms of disorganization. It also predicted evoked theta signal. Conclusion: The substantial reduction of both evoked and induced oscillatory activity in schizophrenia indicates diminished recruitment of brain circuits engaged not only in stimulus-locked perceptual processing but also in more extensive processing less tightly time locked to the stimulus. Although reduced phase resetting makes a lesser contribution, it indicates a deficit in the ability to harness ongoing electrical activity.     

Are obsessional thoughts and worry different cognitive phenomena?

Worry and obsessional thoughts are cognitive activities that can be found in the general population as well as among various psychopathological states. In addition, these two types of cognitive phenomena are among the defining characteristics of two distinct anxiety disorders: generalized anxiety disorder (worry) and obsessive-compulsive disorder (obsessions). Through a review of the literature, the core features of these cognitive phenomena were compared and contrasted in an effort to determine areas of similarities and differences. The conclusion indicates that although there are areas of overlap, obsessions can be differentiated from worry along several important dimensions. Also, adverse mood state appears to play a critical role when both worry and obsessional thoughts are pathological.     

Resting-state EEG theta activity and risk learning: sensitivity to reward or punishment?

Increased theta (4–7 Hz)–beta (13–30 Hz) power ratio in resting state electroencephalography (EEG) has been associated with risky disadvantageous decision making and with impaired reinforcement learning. However, the specific contributions of theta and beta power in risky decision making remain unclear. The first aim of the present study was to replicate the earlier found relationship and examine the specific contributions of theta and beta power in risky decision making using the Iowa Gambling Task. The second aim of the study was to examine whether the relation were associated with differences in reward or punishment sensitivity. We replicated the earlier found relationship by showing a positive association between theta/beta ratio and risky decision making. This correlation was mainly driven by theta oscillations. Furthermore, theta power correlated with reward motivated learning, but not with punishment learning. The present results replicate and extend earlier findings by providing novel insights into the relation between thetabeta ratios and risky decision making. Specifically, findings show that resting-state theta activity is correlated with reinforcement learning, and that this association may be explained by differences in reward sensitivity.     

Is the relationship between frontal EEG alpha asymmetry and depression mediated by implicit or explicit self-esteem?

A robust physiological finding is a higher relative left sided activity in the prefrontal cortex during the experience of positive approach related emotions and a higher relative right sided activity during the experience of negative withdrawal related emotions. Since self-esteem can be conceptualized within a framework of approach/withdrawal tendencies, the present study aimed at investigating if the relation between frontal EEG alpha asymmetry and depressive symptoms is mediated by implicit or explicit self-esteem. Self-esteem was measured by questionnaires (explicit) and in an indirect way (implicit). The mediation analyses showed that only explicit self-esteem acted as a partial mediator in the path from EEG alpha asymmetry to depression.     

Uncomplicated general anesthesia in the elderly results in cognitive decline: Does cognitive decline predict morbidity and mortality?

Elderly surgical patients constitute a unique surgical group. They require special consideration in order to preempt the long term adverse effects of anesthesia. This paper examines the proposition that general anesthesia causes harm to elderly patients with its impact being felt long after the anesthetic agents are cleared from the body. One complication, Postoperative Cognitive Decline (POCD), is associated with the administration of anesthesia and deep sedation. Its' occurrence may herald an increase in morbidity and mortality. Based on both human and animal data, this paper outlines a unitary theoretical framework to explain these phenomena. If this hypothesis proves to be correct, anesthesiologist should consider regional rather than general anesthesia for equivalent surgical procedures to reduce POCD and consequently achieving superior patient outcome.     

Are impaired endothelial progenitor cells involved in the processes of late in-stent thrombosis and re-endothelialization of drug-eluting stents?

Drug-eluting stent (DES) now is the default selection for most of the interventional cardiologists. However, its benefits compromised by the stent-related thrombosis events. Given the catastrophic consequences, it is important to investigate possible mechanisms of stent thrombosis. The cause of stent thrombosis is multifactorial, and several stent-related and patient-related variables have been identified. The stent itself has components that may lead to thrombosis: the metal stent material, the polymer which houses the drug, and the actual cell-cycle inhibiting drugs. Most important the cell-cycle inhibitors (sirolimus and paclitaxel) reduce neointimal formation by impeding smooth muscle cells proliferation and migration, these drugs also impair the normal process of the injured arterial wall and cause delayed re-endothelialization [Tsimikas S. Drug-eluting stents and late adverse clinical outcomes. J Am Coll Cardiol 2006;47:2112-5; Colombo A, Drzewiecki J, Banning A, et al. Randomized study to assess the effectiveness of slow- and moderate-release polymer-based paclitaxel-eluting stent for coronary artery lesions. Circulation 2003;108:788-94; Kedia Gautam, Lee Michael S. Stent thrombosis with drug-eluting stents: a re-examination of the evidence. Catheter Cardiovasc Interv 2007;69:782-9] [1-3]. It has been proposed that bone marrow-derived endothelial progenitor cells may also be involved in re-endothelialization [Urao N, Okigaki M, Yamada H, et al. Erythropoietin-mobilized endothelial progenitors enhance reendothelialization via Akt-endothelial nitric oxide synthase activation and prevent neointimal hyperplasia. Circ Res 2006;98:1405-13; Griese DP, Ehsan A, Melo LG, et al. Isolation and transplantation of autologous circulating endothelial cells into denuded vessels and prosthetic grafts: implications for cell-based vascular therapy. Circulation 2003;108:2710-15] [4-5]. Interestingly, rapamycin inhibits proliferation, migration, and differentiation of human endothelial progenitor cells in vitro [Butzal M, Loges S, Schweizer M, et al. Rapamycin inhibits proliferation and differentiation of human endothelial progenitor cells in vitro. Exp Cell Res 2004;300:65-71; Chen TG, Chen JZ, Wang XX. Effects of rapamycin on number activity and eNOS of endothelial progenitor cells from peripheral blood. Cell Proliferat 2006;39:117-25]. We hypothesis that drugs loaded on DES may affect the number as well as the homing and proliferation of endothelial progenitor cells, thus further preventing proper endothelial healing, increasing platelet aggregation, which could lead to stent thrombosis.     

Shared cognitive processes underlying performance on the Wisconsin Card Sorting Test and the Stroop Test in patients with schizophrenia: A measurement artifact?

We explored the hypothesis that, while sensitive to different aspects of executive functioning in patients with schizophrenia, the Wisconsin Card Sorting Test (WCST) and the Stroop Test also measure the same construct, namely, inhibitory control. Specifically, our goal was to confirm and extend previous findings [A. Rossi, E. Daneluzzo, P. Mattei, M. Bustini, M. Cassachia, P. Stratta, Wisconsin Card Sorting Test and Stroop performance in schizophrenia: a shared construct, Neurosci. Lett. 226 (1997) 87-90] by demonstrating the independence of this construct from other abilities necessary to successfully perform the tasks. More importantly, we sought to improve on this previous study by eliminating the influence of the variance of speed of responding. We examined 55 patients with schizophrenia and initially found that performance on the Stroop Color-Word condition could, indeed, be predicted only by the percentage of perseverative errors on the WCST, and not variables reflective of other cognitive skills, thus replicating and extending previous findings. Once we removed the influence of speed of responding from our measure, however, thus isolating the inhibitory process, this finding disappeared. Therefore, our findings highlight the importance of isolating the individual components of interest from complex measures before drawing conclusions regarding the cognitive processes underlying particular test performance.     

Are all cognitive therapies alike? A comparison of cognitive and noncognitive therapy process and implications for the application of empirically supported treatments

The definition of an empirically supported treatment (EST) arguably embodies 2 untested assumptions: (a) that different manualized renditions of the same therapy are functionally equivalent and (b) that therapies can be reliably applied independently of therapist, setting, and format. These assumptions were tested as applied to cognitive therapy (CT), using process data from a large multisite study (N = 235) that included 3 cognitive and 6 alternative therapies. Although the non-CTs were more variable than the CTs on 2 of 4 dimensions studied (directiveness and emotional arousal), there was considerable variation among the 3 CTs, even when implemented in the current context of rigorous training, manualization, and adherence checks. Results are discussed as related to the assumptions underlying EST criteria.     

Are there reliable changes in memory and executive functions after cognitive behavioural therapy in patients with obsessive-compulsive disorder?

Introduction. Patients with obsessive-compulsive disorder (OCD) have impaired memory and executive functions, but it is unclear whether these functions improve after cognitive behavioural therapy (CBT) of OCD symptoms. The primary aim of this study was to investigate whether memory and executive functions change after CBT in patients with OCD.

Methods. We assessed 39 patients with OCD before and after CBT with neuropsychological tests of memory and executive functions. To correct for practice effects, 39 healthy controls (HCs) were assessed at two parallel time intervals with the neuropsychological tests.

Results. There were no changes in memory and executive functions after CBT in patients with OCD when results were corrected for practice effects. Patients performed worse on a test of visuospatial memory and organisational skills (Rey complex figure test [RCFT]) compared to HCs both before and after CBT (ps = .002–.036).

Conclusions. The finding of persistent poor RCFT performances indicates that patients with OCD have impaired visuospatial memory and organisational skills that may be trait-related rather than state-dependent. These impairments may need to be considered in treatment. Our findings underline the importance of correcting for practice effects when investigating changes in cognitive functions.     

Are tau and alpha synuclein filamentous inclusions in neurons and glia analogous to accumulation of myosin/actin filaments in myofiber hypertrophy?

Degenerative disruption of neuronal networks would appear to constitute a pathogenetic series of mechanisms that would adequately account for the effects of neurodegeneration in its full complexity clinically and pathologically beyond any consideration of the neuron as the basic unit of involvement.In this sense, neurodegeneration as reflected in terms of neurofibrillary tangles and Lewy bodies might actually be a process of integral tau opathy and synucleinopathy that in probably multiple different ways in the individual patient contributes to a disruption of neuronal interactions as an integral neuronal network.In terms therefore of aggregation of neurofilaments or of synuclein filaments it might be valid to consider simple biophysical phenomena of inclusion body formation in neurons directly analogous to myosin/actin accumulation in myofibers in an overall common system of neuronal and myofiber biology and pathobiology.     

Do cognitive, physiological, and psychosocial risk and promotive factors predict desistance from delinquency in males?

Relatively few studies have examined cognitive, physiological, and psychosocial promotive and risk factors that can be linked to desistance from delinquency in community samples. This paper reports on a sample of boys first studied at age 7 and then followed up yearly to age 20. Around age 16, most of the boys received a range of cognitive tests; at that time, information regarding their resting heart rate and skin conductance activity in response to aversive stimuli was also collected. Several psychosocial and two cognitive measures distinguished delinquents from nondelinquents around age 16. Among the promotive factors associated with low delinquency were good housing quality, low community crime (parent and youth report), verbal IQ, delayed verbal memory, and sustained attention. Predictive analyses discriminating between desisters and persisters in delinquency between ages 17 and 20 showed that all of the significant predictors were either child or peer risk factors. None of the cognitive, physiological, parenting, or community factors significantly predicted desistance from delinquency. In addition, no promotive factors were significantly related to desistance. The final set of analyses compared persisters, desisters, and nondelinquents in terms of their adult adjustment. Desisters were similar to persisters in that desisters continued to display serious problems in anxiety, failure to graduate from high school, no post high school education, being a nonstudent and unemployed, daily cigarette use, and weekly marijuana use. Desisters scored low on depression and weekly heavy drinking and in these respects were indistinguishable from nondelinquents and better off than persisters.     

Are chemokines the third major system in the brain?

Chemokines are a family of small proteins involved in cellular migration and intercellular communication. Although the chemokines and their receptors are located throughout the brain, they are not distributed uniformly. Among the chemokines and their receptors that are arrayed disproportionately in glia and neurons are monocyte chemotactic protein-1/CC chemokine ligand 2 (CCL2), stromal cell-derived factor-1/CXC chemokine ligand 12 (CXCL12), fractalkine/CX3C chemokine ligand 1, interferon-gamma-inducible-protein-10/CXCL10, macrophage inflammatory protein-1alpha/CCL3, and regulated on activation, normal T cell expressed and secreted/CCL5. In the brain, they are found in the hypothalamus, nucleus accumbens, limbic system, hippocampus, thalamus, cortex, and cerebellum. The uneven distribution suggests that there may be functional roles for the chemokine "system," comprised of chemokine ligands and their receptors. In addition to anatomical, immunohistochemical, and in vitro studies establishing the expression of the chemokine ligands and receptors, there is an increasing body of research that suggests that the chemokine system plays a crucial role in brain development and function. Our data indicate that the chemokine system can alter the actions of neuronally active pharmacological agents including the opioids and cannabinoids. Combined with evidence that the chemokine system in the brain interacts with neurotransmitter systems, we propose the following hypothesis: The endogenous chemokine system in the brain acts in concert with the neurotransmitter and neuropeptide systems to govern brain function. The chemokine system can thus be thought of as the third major transmitter system in the brain.