Faculty Bibliography

This paper is a contribution to a theory of duration and subjective time in dream and waking consciousness. According to microgenetic theory, an act of thought begins, Wittgenstein wrote, and psychoanalysts would agree, as would I, with instinct as the animal inheritance traverses the evolutionary core of the brain, the drives arousing acquired experience and knowledge. These strands of the inherited and acquired constitute the core self, the "me," which is bound up with bodily function, immediacy and the largely innate determinants of behavior. This construct passes a liminal threshold leading to a conscious self in relation to desire for objects or conditions in the future. Thus, the self appears early in the mental state prior to thought and the endpoint of object-perception. A mental state enfolds a transition from instinct to thought to perception in a fraction of a second. The partial overlap of early segments in a series of mental states arouses preliminary phases out of which thoughts and perceptions actualize. Long-term or experiential memories, revised but not erased by the oncoming state, serve as a foundation for thought and perception, while segments at the surface or endpoint of the state that transition to an object, which are not enfolded in the overlap, are receptive to new perceptions. In dreaming, the specious or illusory present arises in the overlap of mental states and the incomplete revival of their predecessors. Incompleteness of revival is the key to recall as fading states lapse to successive planes of iconic, short- and long-term memory. The present arises in the forgetting of perceptions, or the passage of perceptual to memorial content, as the disparity between the floor of the mental state"“the endpoint of withdrawal beneath recall"“and conscious revival"“the ceiling of the mental state"“in the final actuality. This disparity is converted to a longitudinal epoch of duration. The degree to which each state is revived"“the forgetting of each state, in dream and waking"“accounts for the rapid decay in dream recall on waking, as well as the predominance of imagery.

Unprecedented media coverage of concussion in sport has led to increased fears regarding the potential negative effects of participation in contact sports including North American football and ice hockey. Initial responses of professional sports leagues to implementation of acute concussion management practices and reports of a neurodegenerative condition known as chronic traumatic encephalopathy (CTE) developing in retired players caused an atmosphere of distrust whereby the leagues were accused of maintaining cover-ups analogous to what had been seen in association with studies of tobacco and smoking. This article reviews the important role that psychology has played in the study of sports concussion and in the establishment of methods currently used to diagnose and track concussion symptoms. Results of existing studies have shown that the neurobiological effects of concussion are rather short-lived with development of persisting symptoms in some individuals associated more with psychosocial factors than underlying physiological effects. With regard to CTE, the status of the science remains preliminary with little definitive information known about its epidemiology or cause. In the midst of the ongoing controversy, a polarized climate has developed in association with concussion and CTE, divided by believers in the dangers of long-term consequences and deniers who question the status of the existing science. The conclusion is that it is important for psychology to extend its scope of study to provide increased understanding of the social factors underlying the current polarized climate while continuing to provide the public with an accurate and reliable account of the existing science. (PsycInfo Database Record (c) 2020 APA, all rights reserved)Public Significance Statement"”Continued media reporting of the sports concussion and its potential long-term effects has been accompanied by public concerns about the safety of contact sports and potential development of chronic traumatic encephalopathy (CTE). Controversies have emerged about the status of the science, creating polarization on the topic. Psychology has provided significant contributions to our scientific knowledge on sports concussion and has the potential to provide a key to understanding the factors underlying division on these topics. (PsycInfo Database Record (c) 2020 APA, all rights reserved)Une couverture médiatique sans précédent des commotions cérébrales dans le sport a entraîné une augmentation des craintes quant aux effets négatifs potentiels de la participation aux sports de contact, notamment au football et au hockey sur glace en Amérique du Nord. Les premières réponses des ligues sportives professionnelles à la mise en Å“uvre de pratiques de gestion des commotions aiguës et les déclarations de maladie neurodégénérative connue sous le nom d"™encéphalopathie traumatique chronique (CTE) en développement chez les joueurs retraités ont provoqué une atmosphère de méfiance où les ligues ont été accusées de dissimulations de manière similaire à ce qui avait été observé avec les études sur le tabac et le tabagisme. Le présent article examine le rôle important que la psychologie a joué dans l"™Ã©tude des commotions liées au sport et dans l"™Ã©tablissement de méthodes actuellement utilisées pour diagnostiquer et surveiller les symptômes de commotion cérébrale. Les résultats des études existantes ont montré que les effets neurobiologiques de commotion cérébrale sont plutôt de courte durée avec l"™apparition de symptômes persistants, chez certaines personnes, plutôt associés à des facteurs psychosociaux qu"™aux effets physiologiques sous-jacents. En ce qui concerne la CTE, le statut de la science reste préliminaire, avec peu de renseignements définitifs connus sur son épidémiologie ou sa cause. Au cÅ“ur de la controverse actuelle, un climat polarisé s"™est développé en lien avec la commotion cérébrale et la CTE, divisé par les croyants aux dangers des conséquences à long terme et les négateurs qui remettent en question le statut de la science existante. En conclusion, il est important pour la psychologie d"™Ã©tendre sa portée d"™Ã©tude afin de mieux comprendre les facteurs sociaux sous-jacents au climat polarisé actuel tout en continuant à fournir au public un compte rendu exact et fiable de la science existante. (PsycInfo Database Record (c) 2020 APA, all rights reserved)

Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 μm (PM2.5) may increase the risk for Alzheimer's disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer's disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer's disease associated with exposure. Participants included older females (n = 998; aged 73-87) enrolled in both the Women's Health Initiative Study of Cognitive Aging and the Women's Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999-2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1-3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005-06; MRI-2: 2009-10). Subjects were assigned Alzheimer's disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer's disease), developed by supervised machine learning and validated with data from the Alzheimer's Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 μg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1-3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer's disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1-3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer's disease risk, independent of cerebrovascular damage.

Background/UNASSIGNED:Spinal neurofibromas (SNFs) in neurofibromatosis type 1 (NF1) can cause progressive spinal cord compression and neurological dysfunction. The MEK inhibitor selumetinib shrinks the majority of plexiform neurofibromas (PNs) in patients with NF1. We assessed the effect of selumetinib on SNF. Methods/UNASSIGNED:/dose twice daily (max 50 mg b.i.d.; 1 cycle = 28 days). We qualitatively assessed the effect of selumetinib on SNF-related spinal canal distortion, cerebrospinal fluid distribution, and spinal cord deformity on MRI. Results/UNASSIGNED:Twenty-four patients (18 male), median age 16.9 years (range, 6.2-60.3), had SNF, 22 of which were associated with the same nerves as the target PN assessed on the clinical trial. Twenty patients had spinal cord deformity. Twenty-three patients completed at least 12 treatment cycles to date. Eighteen patients showed subtle to a marked improvement in SNF burden, 5 remained stable, and no worsening was observed during treatment. Conclusions/UNASSIGNED:This is the first study describing the effect of selumetinib on SNF. Of 24 patients, 18 exhibited some improvement of SNF burden on imaging. These findings suggest that selumetinib may prevent the worsening of cord compression, potentially reducing the need for surgical interventions in select patients or benefitting patients who do not have a surgical option. Prospective evaluation of the clinical benefit of selumetinib for SNF is warranted.

Background and Purpose/UNASSIGNED:Many studies supporting the association between specific surgical procedure categories and postoperative stroke (POS) do not account for differences in patient-level characteristics between and within surgical categories. The risk of POS after high-risk procedure categories remains unknown after adjusting for such differences in patient-level characteristics. Methods/UNASSIGNED:Using inpatients in the American College of Surgeons National Surgical Quality Initiative Program database, we conducted a retrospective cohort study between January 1, 2000, and December 31, 2010. Our primary outcome was POS within 30 days of surgery. We characterized the relationship between surgical- and individual patient-level factors and POS by using multivariable, multilevel logistic regression that accounted for clustering of patient-level factors with surgical categories. Results/UNASSIGNED:We identified 729 886 patients, 2703 (0.3%) of whom developed POS. Dependent functional status (odds ratio [OR]: 4.11, 95% confidence interval [95% CI]: 3.60-4.69), history of stroke (OR: 2.35, 95%CI: 2.06-2.69) or transient ischemic attack (OR: 2.49 95%CI: 2.19-2.83), active smoking (OR: 1.20, 95%CI: 1.08-1.32), hypertension (OR: 2.11, 95%CI: 2.19-2.82), chronic obstructive pulmonary disease (OR: 1.39 95%CI: 1.21-1.59), and acute renal failure (OR: 2.35, 95%CI: 1.85-2.99) were significantly associated with POS. After adjusting for clustering, patients who underwent cardiac (OR: 11.25, 95%CI: 8.52-14.87), vascular (OR: 4.75, 95%CI: 3.88-5.82), neurological (OR: 4.60, 95%CI: 3.48-6.08), and general surgery (OR: 1.40, 95%CI: 1.15-1.70) had significantly greater odds of POS compared to patients undergoing other types of surgical procedures. Conclusions/UNASSIGNED:Vascular, cardiac, and neurological surgery remained strongly associated with POS in an analysis accounting for the association between patient-level factors and surgical categories.

Andexanet-alpha is a specific reversal agent for direct factor Xa inhibitors (dFXaI). We aimed to project utilization rates and cost of andexanet for reversal of dFXaI-related major hemorrhage compared to 4-factor prothrombin complex concentrates (4F-PCC). A retrospective, multicenter review was conducted between 1/1/2014 and 7/15/2018 of patients who received 4F-PCC for reversal of dFXaI-related life-threatening hemorrhages. Total hospital reimbursements/patient were calculated based on national average MS-DRG payments adjusting for Medicare discounts. The projected cost for andexanet (based on dose and insurance) and % reimbursement/patient was compared to the actual cost of 4F-PCC. Hemostasis at 24 h (excellent/good vs. poor) and 30-day thrombotic complications were assessed. Of 126 patients who received 4F-PCC to reverse dFXaI, 46 (~ 10 per-year) met inclusion criteria. The median projected cost of andexanet was $22,120/patient, compared to $5670/patient for 4F-PCC (P < 0.001). The median hospital reimbursement was $11,492/hospitalization. The projected cost of andexanet alone would exceed the entire hospital reimbursement in 74% of patients by a median of $7604, while 4F-PCC cost exceeded the total hospital payments in 7% of patients in the same cohort (P < 0.001). Hemostasis was excellent/good in 72% of patients post-4F-PCC, compared to 82% in andexanet trials. Thromboembolic events occurred in 4% of patients following 4F-PCC versus 10% in andexanet trials. The projected cost of andexanet would exceed the national average hospital reimbursement/patient in nearly 75% of patients by over $7500/hospitalization. 4F-PCC was significantly less expensive, had lower rates of thrombosis, but also lower rates of good/excellent hemostasis compared to published data for andexanet.

BACKGROUND:, a double-blind phase III trial in 215 paediatric patients with multiple sclerosis (MS) (10 to <18 years), fingolimod administered for up to 2 years significantly reduced the annualised relapse rate (ARR) and rate of new/newly enlarged T2 (n/neT2) lesions compared with interferon (IFN) β-1a. OBJECTIVES/OBJECTIVE:To investigate (1) differences between treatment groups across subpopulations (treatment-naïve, younger/prepubertal patients); (2) disability progression. METHODS:ARRs at 10, 11 and 12 years were estimated based on predefined modelling extrapolations. Changes in Expanded Disability Status Scale (EDSS), and in 3 month (3M) and 6 month (6M) confirmed disability progression (CDP) were evaluated post hoc. RESULTS:In the treatment-naïve subpopulation, fingolimod reduced ARR and n/neT2 lesions by 85.8% and 53.4%, respectively versus INF β-1a (both p<0.001), compared with 81.9% and 52.6% in the overall population. Model-based ARR reductions in younger patients (≤12 years) were 91.9%-94.6%. Twice as many IFN β-1a-treated than fingolimod-treated patients had worse EDSS scores at study end (20.6% vs 10.5%, p=0.043). Risk reductions in 3M-CDP and 6M-CDP were 77.2% (p=0.007) and 80.2% (p=0.040), respectively. CONCLUSIONS:Fingolimod in paediatric MS was associated with consistent control of disease activity versus IFN β-1a (including treatment-naïve and younger patients) and resulted in less disability progression for up to 2 years. TRIAL REGISTRATION NUMBER/BACKGROUND:NCT01892722.

OBJECTIVE:To assay EEG signal quality recorded with tripolar concentric ring electrodes (TCREs) compared to regular EEG electrodes. METHODS:EEG segments were recorded simultaneously by TCREs and regular electrodes, low-pass filtered at 35 Hz (REG35) and 70 Hz (REG70). Clips were rated blindly by nine electroencephalographers for presence or absence of key EEG features, relative to the "gold-standard" of the clinical report. RESULTS:TCRE showed less EMG artifact (F = 15.4, p < 0.0001). Overall quality rankings were not significantly different. Focal slowing was better detected by TCRE and spikes were better detected by regular electrodes. Seizures (n = 85) were detected by TCRE in 64 cases (75.3%), by REG70 in 75 (88.2%) and REG35 in 69 (81.2%) electrodes. TCRE detected 9 (10.6%) seizures not detected by one of the other 2 methods. In contrast, 14 seizures (16.5%) were not detected by TCRE, but were by REG35 electrodes. Each electrode detected interictal spikes when the other did not. CONCLUSIONS:TCRE produced similar overall quality and confidence ratings versus regular electrodes, but less muscle artifact. TCRE recordings detected seizures in 7% of instances where regular electrodes did not. SIGNIFICANCE/CONCLUSIONS:The combination of the two types increased detection of epileptiform events compared to either alone.