Normal Cognitive Processes Research Articles

Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19.

Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds and infection) alter cellular structures and physiologic processes within the neurovascular unit and contribute to cognitive dysfunction. COVID-19 has posed significant complications during acute and convalescent stages in multiple organ systems, including the brain. Cognitive impairment is a prevalent complication in COVID-19 patients, irrespective of severity of acute SARS-CoV-2 infection. Moreover, overwhelming evidence from in vitro, preclinical and clinical studies has reported SARS-CoV-2-induced pathologies in components of the neurovascular unit that are associated with cognitive impairment. Neurovascular unit disruption alters the neurovascular coupling response, a critical mechanism that regulates cerebromicrovascular blood flow to meet the energetic demands of locally active neurons. Normal cognitive processing is achieved through the neurovascular coupling response and involves the coordinated action of brain parenchymal cells (i.e. neurons and glia) and cerebrovascular cell types (i.e. endothelia, smooth muscle cells and pericytes). However, current work on COVID-19-induced cognitive impairment has yet to investigate disruption of neurovascular coupling as a causal factor. Hence, in this review, we aim to describe SARS-CoV-2's effects on the neurovascular unit and how they can impact neurovascular coupling and contribute to cognitive decline in acute and convalescent stages of the disease. Additionally, we explore potential therapeutic interventions to mitigate COVID-19-induced cognitive impairment. Given the great impact of cognitive impairment associated with COVID-19 on both individuals and public health, the necessity for a coordinated effort from fundamental scientific research to clinical application becomes imperative. This integrated endeavour is crucial for mitigating the cognitive deficits induced by COVID-19 and its subsequent burden in this especially vulnerable population.

Putative cause of seizure-induced cognitive alterations: The oscillatory reconfiguration of seizure network.

The dynamic reconfiguration of network oscillations is connected with cognitive processes. Changes in how neural networks and signaling pathways work are crucial to how epilepsy and related conditions develop. Specifically, there is evidence that prolonged or recurrent seizures may induce or exacerbate cognitive impairment. However, it still needs to be determined how the seizure brain configures its functional structure to shape the battle of strong local oscillations vs. slow global oscillations in the network to impair cognitive function. In this paper, we aim to deduce the network mechanisms underlying seizure-induced cognitive impairment by comparing the evolution of strong local oscillations with slow global oscillations and their link to the resting state of healthy controls. Here, we construct a dynamically efficient network of pathological seizures by calculating the synchrony and directionality of information flow between nine patients' SEEG signals. Then, using a pattern-based method, we found hierarchical modules in the brain's functional network and measured the functional balance between the network's local strong and slow global oscillations. According to the findings, a tremendous rise in strong local oscillations during seizures and an increase in slow global oscillations after seizures corresponded to the initiation and recovery of cognitive impairment. Specifically, during the interictal period, local strong and slow global oscillations are in metastable balance, which is the same as a normal cognitive process and can be switched easily. During the pre-ictal period, the two show a bimodal pattern of separate peaks that cannot be easily switched, and some flexibility is lost. During the seizure period, a single-peak pattern with negative peaks is showcased, and the network eventually transitions to a very intense strong local oscillation state. These results shed light on the mechanism behind network oscillations in epilepsy-induced cognitive impairment. On the other hand, the differential (similarity) of oscillatory reorganization between the local (non) epileptogenic network and the global network may be an emergency protective mechanism of the brain, preventing the spread of pathological information flow to more healthy brain regions.

The M1 muscarinic acetylcholine receptor regulates the surface expression of the AMPA receptor subunit GluA2 via PICK1.

Muscarinic acetylcholine receptors (mAChRs) have been shown to play significant roles in the regulation of normal cognitive processes in the hippocampus, and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) are also involved in these processes. This study aims to explore the mAChR-mediated regulation of AMPARs GluA2 trafficking and to reveal the key proteins and the signaling cascade involved in this process. Primary hippocampal neurons, as cell models, were treated with agonist 77-LH-28-1 and antagonist VU0255035, Fsc231, and APV. C57BL/6J male mice were stereotactically injected with 77-LH-28-1 and Fsc231 to obtain hippocampal slices. The trafficking of GluA2 was detected by surface biotinylation and immunostaining. Activation of M1 mAChRs promoted endocytosis and decreased the postsynaptic localization of the AMPA receptor subunit GluA2 and that phosphorylation of GluA2 at Ser880 was increased by M1 mAChR activity. Fsc231 blocked the endocytosis and postsynaptic localization of GluA2 induced by 77-LH-28-1 without affecting the phosphorylation of Ser880. PICK1 was required for M1 mAChR-mediated GluA2 endocytosis and downstream of phosphorylation of GluA2-Ser880, and the PICK1-GluA2 interaction was essential for M1 mAChR-mediated postsynaptic expression of GluA2. Taken together, our results show a functional correlation of M1 mAChRs with GluA2 and the role of PICK1 in their interplay. The schematic diagram for the modulation of GluA2 trafficking by M1 mAChRs. Activation of M1 mAChRs induces PKC activation, and the interaction of PICK1-GluA2 determines the endocytosis and postsynaptic localization of GluA2.

What Has Metaphysics to Do with Wisdom?

What Has Metaphysics to Do with Wisdom? John Haldane There are two loci of ambiguity in the title of the symposium from which this essay derives—"Is Belief in God Reasonable? Aquinas's Summa contra gentiles in a Contemporary Context."1 The first concerns the opening question, "is belief in God reasonable?" and the second the closing clause "in a contemporary context." I observe this not in the spirit of pedantry, but because I want to consider certain interpretations of what is at issue, ones which may be different from those of other contributors but which are relevant to Aquinas's circumstances and interests and to ours. So far as the Summa contra gentiles [SCG] is concerned, I will touch mainly on issues discussed by Thomas at the outset of book I, in chapters 1–15, which deal with philosophical knowledge of first principles and arguments to the existence of God. First, however, the general issue of reasonable belief. I Concerning the first locus of ambiguity, the question of the reasonability of belief in God is multiply interpretable. It may be treated as relative to a subject's other beliefs and attitudes, where that subject e may be an individual or a group. Given that S believes p and q (and these can each be conjunctions of any number of propositions), is it reasonable for S to believe r? This aspect of relative credibility is itself ambiguous because it [End Page 1249] can be viewed narrowly, without regard to the status of those antecedent beliefs and attitudes, or broadly, as also asking whether those are themselves reasonable. In a court setting, for example, it may be asked whether it was reasonable for someone to have believed (or done) something given their antecedent beliefs, but it may well be countered that this is an insufficient standard of reasonability, since the prior attitudes may be incredible, or credible but irresponsibly held. The issue of reasonable belief, foresight and foreseeability are common courtroom examples. In these respects, then, it may be granted by someone A, who holds that believing in God is not reasonable, that it was nevertheless reasonable for S to do so given S's antecedent beliefs. This need not be a matter of condescension, however, since A may grant that the prior beliefs were themselves reasonable for S to hold, and would also have been reasonable by some more objective standard prevailing at the time or in the circumstances. A "rationalist" objector may counter, however, that this is all beside the point, since the question to consider is not the relative, but the absolute one: is belief in God reasonable? Full stop. I agree that there is nothing to be gained by unconstrained relativizing, but if "absolutism" is the implied contrast, it is over-stated. First, if reasonability is related to having (or having access to) reasons, and to the "quality" of those reasons, then some degree of relativity is entailed, and the only standard of reasonability that can be applied is a contextual one. To ask simpliciter whether it is reasonable to believe p carries an unacknowledged implicit reference either to something such as prevailing commonly held beliefs and associated normal cognitive processes or to an idealized thinker with access to relevant proofs or evidence. On further consideration, however, the latter, somewhat like Adam Smith's "impartial spectator" in ethics,2 tends just to be a more abstract version of the contextually reasonable thinker. There is perhaps a step beyond this, namely to the Omniscient Reasoner (OR) but it is a sophistical move, since it amounts to saying that a belief is reasonable if and only if it would be held by someone who knows everything relevant to its justification. which given that we cannot know antecedently the range of relevant considerations, is for us an inapplicably high standard. There is also some irony in asking if OR would judge belief in God Reasonable since OR would be God or at least God-like in respect of being all-knowing. [End Page 1250] II The other respect in which the question "is belief in God reasonable?" is ambiguous (in this first of the two areas ambiguity noted at the...

Religion as Mental Short-Circuit

By identifying religion as schema and attribution process, the first two following sections of the essay argues that religions and cults short-circuit normal cognitive process, bypassing the objective evidence and logical argument inconsistent with the belief system. In the last two sections, the essay demonstrates that recognizing religious thinking mode as a mental short-circuit can be extended to the broader application in human cognition. What’s more, the essay examines the perspective of believers who prioritize the fulfillment of their psychological needs over the righteousness of the logic and calls on building new healthy connections with previous victims in cults instead of spending major effort convincing them of the logic flaw in their previous belief.

An Exploratory Study of Cognitive Involvement in Hereditary Transthyretin Amyloidosis.

Hereditary amyloidogenic transthyretin (ATTRv) amyloidosis is an autosomal dominant disorder caused by mutations of the transthyretin (TTR) gene. The mutant ATTRv protein causes a systemic accumulation of amyloid fibrils in various organs. TTR is an important protein in the central nervous system physiology for the maintenance of normal cognitive process during aging, amidated neuropeptide processing, and nerve regeneration. The neuroprotective effect of transthyretin has been widely documented in animal models. Cognitive consequences of the mutant TTR in hereditary ATTRv amyloidosis patients remain still to be elucidated. We designed this study to investigate the cognitive involvement in ATTRv amyloidosis. Detailed neuropsychological tests and cranial MRIs were performed. Biomarkers including amyloid beta 1-42, total tau, and phosphorylated tau were investigated in the cerebrospinal fluid samples. Median age of the cohort was 52years (ranges 34-72). Neuropsychological assessment results were compatible with impaired executive functions (in all patients except one with only bilateral carpal tunnel syndrome, long-term visual and long-term verbal memory (severe in four patients and moderate in one). Visuospatial judgment and perception were impaired in six. Mean cerebrospinal fluid Aβ1-42 (pg/ml) was 878.0±249.5 in patients with cortical atrophyin MRI whereas 1210.0±45.9 in patients without any cortical atrophy. Cranial MRI showed cortical atrophy in six patients (6/10). Our data showed the significance of the TTR protein in cognitive functions and highlighted the importance of the close follow-up of cognitive functions in ATTRv amyloidosis patients.

Transition to synchronization in heterogeneous inhibitory neural networks with structured synapses.

Inhibitory neurons form an extensive network involved in the development of different rhythms in the cerebral cortex. A transition from an incoherent state, where all inhibitory neurons fire unrelated to each other, to a synchronized or locked state, where all or most neurons define a tight firing pattern, is maybe the most salient process to analyze when considering neuronal rhythms. In this work, we analyzed whether different patterns of effective synaptic connectivity may support a first-order-like transition in this path to synchronization. Such an "explosive" phenomenon may be relevant in neural processes, as normal cognitive processing in different tasks and some neurological disorders manifest an increased power in many neuronal rhythms, supported by an extended concerted spiking activity and an abrupt change to this state. Furthermore, we built an adaptive mechanism that supports the generation of this kind of network, which rapidly creates the underlying structure based on the ongoing firing statistics.

Interplay of Good Bacteria and Central Nervous System: Cognitive Aspects and Mechanistic Considerations.

The human gastrointestinal tract hosts trillions of microorganisms that is called “gut microbiota.” The gut microbiota is involved in a wide variety of physiological features and functions of the body. Thus, it is not surprising that any damage to the gut microbiota is associated with disorders in different body systems. Probiotics, defined as living microorganisms with health benefits for the host, can support or restore the composition of the gut microbiota. Numerous investigations have proved a relationship between the gut microbiota with normal brain function as well as many brain diseases, in which cognitive dysfunction is a common clinical problem. On the other hand, increasing evidence suggests that the existence of a healthy gut microbiota is crucial for normal cognitive processing. In this regard, interplay of the gut microbiota and cognition has been under focus of recent researches. In the present paper, I review findings of the studies considering beneficial effects of either gut microbiota or probiotic bacteria on the brain cognitive function in the healthy and disease statuses.

Assessment of Karnofsky (KPS) and WHO (WHO-PS) performance scores in brain tumour patients: the role of clinician bias.

Inclusion of brain tumour patients in oncological protocols may be hampered by their neurological impairment. The goal of this study was to assess the reliability of Karnofsky Performance Scale (KPS) and WHO Performance Scale (WHO-PS) scores in this population. A cross-sectional survey was conducted through the Association des Neuro-Oncologues d'Expression Française (ANOCEF) and European Neuro-Oncology Association (EANO) networks. Clinicians were asked to write a text defining their operative definition of a patient with ≥ 70 KPS and to assess KPS and WHO-PS in six different clinical case vignettes. Two hundred seventy-six clinicians sent a response. The operative definition mentioned a normal life (89%), what patients were able (26%) or unable (29%) to do, normal cognitive processing (8%) and caregivers (6%). Older physicians mentioned more often what patients were unable to do (p = 0.005). The two scales were homogeneous in less severely handicapped patients only. More patients were excluded for hemiplegia than for expressive aphasia. Older physicians significantly excluded more patients for KPS and WHO-PS. Speciality of the physician significantly influenced scoring. On multivariable analysis, age and speciality of the physicians were correlated with KPS and WHO-PS rating even if adjusted on cases. Discordant scoring increased with severity of the deficit: in nearly all cases, the KPS would have denied, while WHO-PS would have allowed, access to a trial. Performance scores assigned to brain tumour patients are clinician and score dependant. WHO-PS would allow more access to a trial. Specific criteria should be developed for patients with neurological deficits to facilitate their access to trials.

N-Acetylcysteine Inhibits Kynurenine Aminotransferase II

The tryptophan metabolite kynurenic acid (KYNA) may play an important role in normal and abnormal cognitive processes, most likely by interfering with α7 nicotinic and NMDA receptor function. KYNA is formed from its immediate precursor kynurenine either by non-enzymatic oxidation or through irreversible transamination by kynurenine aminotransferases. In the mammalian brain, kynurenine aminotransferase II (KAT II) is the principal enzyme responsible for the neosynthesis of rapidly mobilizable KYNA, and therefore constitutes an attractive target for pro-cognitive interventions. N-acetylcysteine (NAC), a brain-penetrant drug with pro-cognitive efficacy in humans, has been proposed to exert its actions by increasing the levels of the anti-oxidant glutathione (GSH) in the brain. We report here that NAC, but not GSH, inhibits KAT II activity in brain tissue homogenates from rats and humans with IC50 values in the high micromolar to low millimolar range. With similar potency, the drug interfered with the de novo formation of KYNA in rat brain slices, and NAC was a competitive inhibitor of recombinant human KAT II (Ki: 450 μM). Furthermore, GSH failed to S-glutathionylate recombinant human KAT II treated with the dithiocarbamate drug disulfiram. Shown by microdialysis in the prefrontal cortex of rats treated with kynurenine (50 mg/kg, i.p.), peripheral administration of NAC (500 mg/kg, i.p., 120 and 60 min before the application of kynurenine) reduced KYNA neosynthesis by ∼50%. Together, these results suggest that NAC exerts its neurobiological effects at least in part by reducing cerebral KYNA formation via KAT II inhibition.

Delusions and theories of belief.

Cognitive neuropsychiatry is a branch of cognitive psychology that seeks to explain neuropsychiatric symptoms in terms of disruptions or damage to normal cognitive processes. A key objective of this approach is to use insights derived from the study of pathological symptoms to inform accounts of premorbid cognitive systems. Delusions, in particular, can be considered to represent dysfunction of the cognitive processes underlying belief formation, so studying delusions may provide unique insights into nonpathological belief. While this approach has provided compelling accounts for a range of delusions in terms of putative cognitive dysfunctions, it is less clear that it has achieved progress in its reciprocal goal of informing understanding of belief more generally. In this review, we trace the origins of the cognitive neuropsychiatric approach and consider the reasons for the lack of progress. We propose a tentative framework to overcome these challenges and suggest directions for future research.

Facts only the perpetrator could have known? A study of contamination in mock crime interrogations.

This paper examines contamination in interrogations: the process by which an interrogator divulges privileged information to a suspect. In Experiment 1, we predicted that mock investigators would communicate critical crime details when they interview mock suspects about a crime-and that innocent and guilty suspects alike would later produce confessions that contained these details. In Experiment 2, we hypothesized that observers who listened only to the confessions would exhibit a greater guilt bias than those who also had exposure to the eliciting interview. Experiment 1 (N = 59) used student participants in a mock crime scenario to test whether contamination is natural to communication even in the absence of external incentives. In Experiment 2, MTurk participants (N = 499) listened to audio-clips from Experiment 1 to test whether presenting observers with the full interview decreases guilt ratings for false confessors. Investigators divulged crime information to both innocent and guilty suspects, and even false confessions later included accurate details. Although Experiment 2 observers exhibited a guilt bias, exposure to the interview (not just the confession) attenuated this effect for innocent confessors. The information disclosure associated with contamination is a normal cognitive process that occurs even without external incentives to secure a confession. Experiment 2 showed that seeing contamination in action may decrease judgments of guilt for innocent suspects. Interrogations should be recorded in their entirety to provide fact finders with an objective record of the source of crime details contained within narrative confessions. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Dopamine and Noradrenaline in the Brain; Overlapping or Dissociate Functions?

Dopamine and noradrenaline are crucial neuromodulators controlling brain states, vigilance, action, reward, learning, and memory processes. Ventral tegmental area (VTA) and Locus Coeruleus (LC) are canonically described as the main sources of dopamine (DA) and noradrenaline (NA) with dissociate functions. A comparison of diverse studies shows that these neuromodulators largely overlap in multiple domains such as shared biosynthetic pathway and co-release from the LC terminals, convergent innervations, non-specificity of receptors and transporters, and shared intracellular signaling pathways. DA–NA interactions are mainly studied in prefrontal cortex and hippocampus, yet it can be extended to the whole brain given the diversity of catecholamine innervations. LC can simultaneously broadcast both dopamine and noradrenaline across the brain. Here, we briefly review the molecular, cellular, and physiological overlaps between DA and NA systems and point to their functional implications. We suggest that DA and NA may function in parallel to facilitate learning and maintain the states required for normal cognitive processes. Various signaling modules of NA and DA have been targeted for developing of therapeutics. Understanding overlaps of the two systems is crucial for more effective interventions in a range of neuropsychiatric conditions.

Cognitive aging of bipolar patients

Bipolar disorder is a severe, recurrent mood disorder, associated with a higher rate of morbidity and mortality. A new population of aging bipolar patients is emerging for which specific studies are scarce. There seem to be an association between bipolar disorder and major cognitive disorder, significantly affecting patients' psychosocial outcomes. Though the neuropathological mecanisms underlying such an evolution have yet to be found, there are three paradigms that can help us understand the clinical heterogeneity within the aging bipolar group. First, there seem to be different cognitive endophenotypes within the bipolar spectrum, related to different neurodevelopmental abnormalities. Each of these endophenotypes will interact with the normal cognitive aging process which is associated with a decline in certain cognitive domains while others remain stable. Nevertheless this cognitive decline will be variable from one patient to another. This can be explained by cognitive reserve which reflects the brain's capacity to endure neuropathology, and minimize clinical manifestations. The second hypothesis is the neuroprogression paradigm that offers an explanation on how a cyclic disorder such as bipolar disorder could evolve progressively into a major cognitive disorder. According to this paradigm, each manic and depressive episode is associated to an allostatic load, a systemic response associated with the secretion of neuroinflammatory factors which will secondarily alter the brain's connectivity. The third paradigm suggests that bipolar patients may develop either vascular dementia which is coherent with their increased vascular risk factor or another neurodegenerative disease. All three paradigms are not exclusive, and many other factors are to be taken into account such as medication, sensory impairment, health related changes and residual mood symptoms, which can alter cognitive functions.

Absence of gut microbiota during early life affects anxiolytic Behaviors and monoamine neurotransmitters system in the hippocampal of mice

The gut microbiome is composed of an enormous number of microorganisms, generally regarded as commensal bacteria. Resident gut bacteria are an important contributor to health and significant evidence suggests that the presence of healthy and diverse gut microbiota is important for normal cognitive and emotional processing. Here we measured the expression of monoamine neurotransmitter-related genes in the hippocampus of germ-free (GF) mice and specific-pathogen-free (SPF) mice to explore the effect of gut microbiota on hippocampal monoamine functioning. In total, 19 differential expressed genes (Htr7, Htr1f, Htr3b, Drd3, Ddc, Maob, Tdo2, Fos, Creb1, Akt1, Gsk3a, Pik3ca, Pla2g5, Cyp2d22, Grk6, Ephb1, Slc18a1, Nr4a1, Gdnf) that could discriminate between the two groups were identified. Interestingly, GF mice displayed anxiolytic-like behavior compared to SPF mice, which were not reversed by colonization with gut microbiota from SPF mice. Besides, colonization of adolescent GF mice by gut microbiota was not sufficient to reverse the altered gene expression associated with their GF status. Taking these findings together, the absence of commensal microbiota during early life markedly affects hippocampal monoamine gene-regulation, which was associated with anxiolytic behaviors and monoamine neurological signs.

Regulation of cholinergic basal forebrain development, connectivity, and function by neurotrophin receptors.

Cholinergic basal forebrain (cBF) neurons are defined by their expression of the p75 neurotrophin receptor (p75NTR) and tropomyosin-related kinase (Trk) neurotrophin receptors in addition to cholinergic markers. It is known that the neurotrophins, particularly nerve growth factor (NGF), mediate cholinergic neuronal development and maintenance. However, the role of neurotrophin signalling in regulating adult cBF function is less clear, although in dementia, trophic signalling is reduced and p75NTR mediates neurodegeneration of cBF neurons. Here we review the current understanding of how cBF neurons are regulated by neurotrophins which activate p75NTR and TrkA, B or C to influence the critical role that these neurons play in normal cortical function, particularly higher order cognition. Specifically, we describe the current evidence that neurotrophins regulate the development of basal forebrain neurons and their role in maintaining and modifying mature basal forebrain synaptic and cortical microcircuit connectivity. Understanding the role neurotrophin signalling plays in regulating the precision of cholinergic connectivity will contribute to the understanding of normal cognitive processes and will likely provide additional ideas for designing improved therapies for the treatment of neurological disease in which cholinergic dysfunction has been demonstrated.

The expression of the distal dystrophin isoforms Dp140 and Dp71 in the human epileptic hippocampus in relation to cognitive functioning.

Dystrophin is an important protein within the central nervous system. The absence of dystrophin, characterizing Duchenne muscular dystrophy (DMD), is associated with brain related comorbidities such as neurodevelopmental (e.g., cognitive and behavioural) deficits and epilepsy. Especially mutations in the downstream part of the DMD gene affecting the dystrophin isoforms Dp140 and Dp71 are found to be associated with cognitive deficits. However, the function of Dp140 is currently not well understood and its expression pattern has previously been implicated to be developmentally regulated. Therefore, we evaluated Dp140 and Dp71 expression in human hippocampi in relation to cognitive functioning in patients with drug-resistant temporal lobe epilepsy (TLE) and post-mortem controls. Hippocampal samples obtained as part of epilepsy surgery were quantitatively analyzed by Western blot and correlations with neuropsychological test results (i.e., memory and intelligence) were examined. First, we demonstrated that the expression of Dp140 does not appear to differ across different ages throughout adulthood. Second, we identified an inverse correlation between memory loss (i.e., verbal and visual memory), but not intelligence (i.e., neither verbal nor performance), and hippocampal Dp140 expression. Finally, patients with TLE appeared to have similar Dp140 expression levels compared to post-mortem controls without neurological disease. Dp140 may thus have a function in normal cognitive (i.e., episodic memory) processes.

Noise-Assisted Multivariate EMD-Based Mean-Phase Coherence Analysis to Evaluate Phase-Synchrony Dynamics in Epilepsy Patients.

Spatiotemporal evolution of synchrony dynamics among neuronal populations plays an important role in decoding complicated brain function in normal cognitive processing as well as during pathological conditions such as epileptic seizures. In this paper, a non-linear analytical methodology is proposed to quantitatively evaluate the phase-synchrony dynamics in epilepsy patients. A set of finite neuronal oscillators was adaptively extracted from a multi-channel electrocorticographic (ECoG) dataset utilizing noise-assisted multivariate empirical mode de-composition (NA-MEMD). Next, the instantaneous phases of the oscillatory functions were extracted using the Hilbert transform in order to be utilized in the mean-phase coherence analysis. The phase-synchrony dynamics were then assessed using eigenvalue decomposition. The extracted neuronal oscillators were grouped with respect to their frequency range into wideband (1-600 Hz), ripple (80-250 Hz), and fast-ripple (250-600 Hz) bands in order to investigate the dynamics of ECoG activity in these frequency ranges as seizures evolve. Drug-refractory patients with frontal and temporal lobe epilepsy demonstrated a reduction in phase-synchrony around seizure onset. However, the network phase-synchrony started to increase toward seizure end and achieved its maximum level at seizure offset for both types of epilepsy. This result suggests that hyper-synchronization of the epileptic network may be an essential self-regulatory mechanism by which the brain terminates seizures.

Cognitive Biases in Cannabis, Opioid, and Stimulant Disorders: A Systematic Review.

Background: Opiates, cannabis, and stimulants are highly abused and are prevalent disorders. Psychological interventions are crucial given that they help individuals maintain abstinence following a lapse or relapse into substance use. The dual-process theory has posited that while the repeated use of a substance leads to increased automatic processing and increased automatic tendencies to approach substance-specific cues, in addition to the inhibition of other normal cognitive processes. Prior reviews are limited, as they failed to include trials involving participants with these prevalent addictive disorders or have not reviewed the published literature extensively.Objectives: The primary aim of this review is to synthesize the evidence for cognitive biases in opioid use, cannabis use, and stimulant use disorders. The secondary aim of the review is to determine if cognitive bias could be consistently detected using the different methods. Lastly, this review will narratively synthesize the evidence of possible associations between cognitive biases and other addiction-related outcomes.Methods: A search was conducted from November 2017 to January 2018 on PubMed, MEDLINE, Embase, PsycINFO, Science Direct, Cochrane Central, and Scopus. Articles were included if participants had a primary diagnosis of opioid use, cannabis use, or stimulant use disorder. The selection process of the articles was in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. A qualitative synthesis was undertaken.Results: A total of 38 studies were identified. The main finding is the evidence that cognitive biases are present in the 38 studies identified, except for a single study on opioid use and stimulant use disorders. Cognitive biases were reported despite a variety of different methods being utilized. Synthesis of secondary outcome was not feasible, due to the varied outcomes reported.Conclusions: Cognitive biases have been consistently observed in opioid use, cannabis use, and stimulant use disorders, despite a range of assessment tools being utilized in the assessment for these biases.

(191) - Driving behavior in chronic low back pain: a preliminary self-report study

CLBP is one of the most common and costly medical conditions in the US, with a three month prevalence of about one-third. In addition to CLBP's sensory and emotional effects, pain demands attention in order to warn of bodily harm and prevent further injury. Although this is a functional response in the short term in chronic states, this pain attention can become debilitating, interfering with normal cognitive processes, and could potentially interfere with common daily tasks. The effect of pain on daily cognitive tasks has been considered in a number of domains, however, the key task of driving is presently underrepresented. Millions of US citizens are injured in car crashes annually, but it is not known if pain patients are at greater risk or how these individuals experience the task of driving. Three hundred and fifteen CLBP patients (159 female, Mage 35.16 years, SD 10.52) were given an online survey and compensated through Mturk. Self-reported pain and vehicle collisions over the past year were taken from the survey, as were measures of driving behavior, mood, and cognition. Findings suggested that pain was not associated with vehicle collisions. However, patients did report feeling more distracted, irritable, and impatient behind the wheel with increasing pain intensity. While collisions were not found to be associated with chronic low back pain, there is still a need to understand how driving experience is different for these patients. Further research is needed to more adequately study techniques performed by these patients while driving to combat their pain, such as sitting posture. The results show that certain cognitive processes and emotional states are associated with pain, so a better understanding of chronic low back pain patients' driving experience is paramount in developing new strategies to help lessen the impact of chronic low back pain on the driver.