rudyvdbrink/CitationDatabase huggingface dataset:
Relationships between nonappearance self-discrepancy, weight discrepancy, and binge eating disorder symptoms.
Eating and weight disorders : EWD, 2021

Self-discrepancy (i.e., perceived differences between one's actual self and personal standards) has been associated with binge eating disorder (BED) symptoms. However, little is known about how weight discrepancy (i.e., the difference between one's actual and ideal weights) interacts with or is distinguished from nonappearance self-discrepancy (discrepancy unrelated to weight or shape) in predicting BED severity. The current study examined how these two forms of discrepancy independently and interactively relate to BED and associated symptoms to elucidate how facets of self-discrepancy may operate to precipitate and maintain BED.
Validity of cluster headache diagnoses in an electronic health record data repository.
Headache, 2016

Cluster headache (CH) is uncommon, so electronic searches of large medical record databases provide an important opportunity to identify a sufficient number of patients for research, patient registries, or quality improvement work. However, the accuracy of CH diagnoses recorded in electronic health record (EHR) databases is unknown. The Research Patient Data Registry (RPDR) warehouses information from EHR of two academic medical centers in Boston. We assessed the validity of CH diagnoses in the RPDR as well as the sensitivity of International Classification of Headache Disorders (ICHD) diagnostic criteria in relation to the gold standard of expert clinician diagnosis of CH.
Autistic traits, but not schizotypy, predict increased weighting of sensory information in Bayesian visual integration.
eLife, 2018

Recent theories propose that schizophrenia/schizotypy and autistic spectrum disorder are related to impairments in Bayesian inference that is, how the brain integrates sensory information (likelihoods) with prior knowledge. However existing accounts fail to clarify: (i) how proposed theories differ in accounts of ASD vs. schizophrenia and (ii) whether the impairments result from weaker priors or enhanced likelihoods. Here, we directly address these issues by characterizing how 91 healthy participants, scored for autistic and schizotypal traits, implicitly learned and combined priors with sensory information. This was accomplished through a visual statistical learning paradigm designed to quantitatively assess variations in individuals' likelihoods and priors. The acquisition of the priors was found to be intact along both traits spectra. However, autistic traits were associated with more veridical perception and weaker influence of expectations. Bayesian modeling revealed that this was due, not to weaker prior expectations, but to more precise sensory representations.
Crucial role of astrocytes in temporal lobe epilepsy.
Neuroscience, 2016

Astrocytes sense and respond to synaptic activity through activation of different neurotransmitter receptors and transporters. Astrocytes are also coupled by gap junctions, which allow these cells to redistribute through the glial network the K(+) ions excessively accumulated at sites of intense neuronal activity. Work over the past two decades has revealed important roles for astrocytes in brain physiology, and it is therefore not surprising that recent studies unveiled their involvement in the etiology of neurological disorders such as epilepsy. Investigation of specimens from patients with pharmacoresistant temporal lobe epilepsy and epilepsy models revealed alterations in expression, localization and function of astrocytic connexins, K(+) and water channels. In addition, disturbed gliotransmission as well as malfunction of glutamate transporters and of the astrocytic glutamate- and adenosine-converting enzymes - glutamine synthetase and adenosine kinase, respectively - have been observed in epileptic tissues. Accordingly, increasing evidence indicates that dysfunctional astrocytes are crucially involved in processes leading to epilepsy. These new insights might foster the search for new targets for the development of new, more efficient anti-epileptogenic therapies.
Metabotropic glutamate receptors and fragile x mental retardation protein: partners in translational regulation at the synapse.
Science signaling, 2008

Fragile X syndrome (FXS) mental retardation is caused by loss-of-function mutations in an RNA-binding protein, fragile X mental retardation protein (FMRP). Previous studies in patients or animal models of FXS have identified alterations in dendritic spine structure, as well as synaptic plasticity induced by metabotropic glutamate receptors (mGluRs). The translation of multiple messenger RNA (mRNA) targets of FMRP is regulated by mGluRs at synapses. Here, we incorporate data from several studies into a working model of how FMRP regulates mGluR-stimulated protein synthesis and, in turn, regulates protein synthesis-dependent synaptic plasticity. Understanding the complex functions of FMRP at the synapse will lead to a better understanding of the neurobiological underpinnings of mental retardation.
Advances in diagnosis, classification, pathophysiology, and management of trigeminal neuralgia.
The Lancet. Neurology, 2020

Trigeminal neuralgia is a very painful neurological condition with severe, stimulus-evoked, short-lasting stabbing pain attacks in the face. The past decade has offered new insights into trigeminal neuralgia symptomatology, pathophysiology, and treatment, leading to a change in the classification of the condition. An accurate diagnosis is crucial because neuroimaging interpretation and clinical management differ among the various forms of facial pain. MRI using specific sequences should be a part of the diagnostic workup to detect a possible neurovascular contact and exclude secondary causes. Demonstration of a neurovascular contact should not be used to confirm a diagnosis but rather to facilitate surgical decision making. Carbamazepine and oxcarbazepine are drugs of first choice for long-term treatment, whereas microvascular decompression is the first-line surgery in medically refractory patients. Advances in neuroimaging techniques and animal models will provide further insight into the causes of trigeminal neuralgia and its pathophysiology. Development of more efficacious treatment options is highly warranted.
Acute seizures in acute ischemic stroke: does thrombolysis have a role to play?
Journal of neurology, 2013

Seizures appear at stroke presentation, during the acute phase or as a late complication of stroke. Thrombolysis has not been investigated as a risk factor despite its potential neurotoxic effect. We try to identify risk factors for seizures during the acute phase of ischemic stroke in a cohort including thrombolysed patients. We undertook a case-control study at a single stroke center using data from Acute Stroke Registry and Analyse of Lausanne (ASTRAL). Patients with seizure occurring during the first 7 days following stroke were retrospectively identified. Bi-variable and multivariable statistical analyses were applied to compare cases and randomly selected controls. We identified 28 patients experiencing from seizures in 2,327 acute ischemic strokes (1.2 %). All seizures occurred during the first 72 h. Cortical involvement, thrombolysis with rt-PA, arterial recanalization, and higher initial NIHSS were statistically associated with seizures in univariated analysis. Backward linear regression identified cortical involvement (OR 7.53, 95 % CI 1.6-35.2, p < 0.01) and thrombolysis (OR 4.6, 95 % CI 1.6-13.4, p = 0.01) as being independently associated with seizure occurrence. Overall, 3-month outcome measured by the modified Rankin scale (mRS) was comparable in both groups. In the subgroup of thrombolysed patients, outcome was significantly worse at 3 months in the seizure group with 9/12 (75 %) patients with mRS ≥ 3, compared to 6/18 (33.3 %) in the seizure-free group (p = 0.03). Acute seizures in acute ischemic stroke were relatively infrequent. Cortical involvement and thrombolysis with rt-PA are the principal risk factors. Seizures have a potential negative influence on clinical outcome in thrombolysed patients.
Audibility, speech perception and processing of temporal cues in ribbon synaptic disorders due to OTOF mutations.
Hearing research, 2015

Mutations in the OTOF gene encoding otoferlin result in a disrupted function of the ribbon synapses with impairment of the multivesicular glutamate release. Most affected subjects present with congenital hearing loss and abnormal auditory brainstem potentials associated with preserved cochlear hair cell activities (otoacoustic emissions, cochlear microphonics [CMs]). Transtympanic electrocochleography (ECochG) has recently been proposed for defining the details of potentials arising in both the cochlea and auditory nerve in this disorder, and with a view to shedding light on the pathophysiological mechanisms underlying auditory dysfunction. We review the audiological and electrophysiological findings in children with congenital profound deafness carrying two mutant alleles of the OTOF gene. We show that cochlear microphonic (CM) amplitude and summating potential (SP) amplitude and latency are normal, consistently with a preserved outer and inner hair cell function. In the majority of OTOF children, the SP component is followed by a markedly prolonged low-amplitude negative potential replacing the compound action potential (CAP) recorded in normally-hearing children. This potential is identified at intensities as low as 90 dB below the behavioral threshold. In some ears, a synchronized CAP is superimposed on the prolonged responses at high intensity. Stimulation at high rates reduces the amplitude and duration of the prolonged potentials, consistently with their neural generation. In some children, however, the ECochG response only consists of the SP, with no prolonged potential. Cochlear implants restore hearing sensitivity, speech perception and neural CAP by electrically stimulating the auditory nerve fibers. These findings indicate that an impaired multivesicular glutamate release in OTOF-related disorders leads to abnormal auditory nerve fiber activation and a consequent impairment of spike generation. The magnitude of these effects seems to vary, ranging from no auditory nerve fiber activation to an abnormal generation of EPSPs that occasionally trigger a synchronized electrical activity, resulting in high-threshold CAPs.
Two Independent Frontal Midline Theta Oscillations during Conflict Detection and Adaptation in a Simon-Type Manual Reaching Task.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017

One of the most firmly established factors determining the speed of human behavioral responses toward action-critical stimuli is the spatial correspondence between the stimulus and response locations. If both locations match, the time taken for response production is markedly reduced relative to when they mismatch, a phenomenon called the Simon effect. While there is a consensus that this stimulus-response (S-R) conflict is associated with brief (4-7 Hz) frontal midline theta (fmθ) complexes generated in medial frontal cortex, it remains controversial (1) whether there are multiple, simultaneously active theta generator areas in the medial frontal cortex that commonly give rise to conflict-related fmθ complexes; and if so, (2) whether they are all related to the resolution of conflicting task information. Here, we combined mental chronometry with high-density electroencephalographic measures during a Simon-type manual reaching task and used independent component analysis and time-frequency domain statistics on source-level activities to model fmθ sources. During target processing, our results revealed two independent fmθ generators simultaneously active in or near anterior cingulate cortex, only one of them reflecting the correspondence between current and previous S-R locations. However, this fmθ response is not exclusively linked to conflict but also to other, conflict-independent processes associated with response slowing. These results paint a detailed picture regarding the oscillatory correlates of conflict processing in Simon tasks, and challenge the prevalent notion that fmθ complexes induced by conflicting task information represent a unitary phenomenon related to cognitive control, which governs conflict processing across various types of response-override tasks.
Deep molecular diversity of mammalian synapses: why it matters and how to measure it.
Nature reviews. Neuroscience, 2012

Pioneering studies in the middle of the twentieth century revealed substantial diversity among mammalian chemical synapses and led to a widely accepted classification of synapse type on the basis of neurotransmitter molecule identity. Subsequently, powerful new physiological, genetic and structural methods have enabled the discovery of much deeper functional and molecular diversity within each traditional neurotransmitter type. Today, this deep diversity continues to pose both daunting challenges and exciting new opportunities for neuroscience. Our growing understanding of deep synapse diversity may transform how we think about and study neural circuit development, structure and function.
Task- and response related dissociations between neglect in near and far space: a morphometric case study.
Behavioural neurology, 2013

Patients with unilateral neglect may show line bisection errors selectively in either near (within hand reaching) or far (beyond hand reaching) space which suggests that these two spatial areas are coded differently by the brain. This exploratory study investigated, whether any difference in performance between these spatial domains might be task-independent or modulated by the requirement for a motor response.
Effects of γ-Aminobutyric Acid Type A Receptor Modulation by Flumazenil on Emergence from General Anesthesia.
Anesthesiology, 2016

Transitions into conscious states are partially mediated by inactivation of sleep networks and activation of arousal networks. Pharmacologic hastening of emergence from general anesthesia has largely focused on activating subcortical monoaminergic networks, with little attention on antagonizing the γ-aminobutyric acid type A receptor (GABAAR). As the GABAAR mediates the clinical effects of many common general anesthetics, the authors hypothesized that negative GABAAR modulators would hasten emergence, possibly via cortical networks involved in sleep.
Manifestation of Lambert-Eaton myasthenic syndrome during last trimester of pregnancy.
The International journal of neuroscience, 2010

Lambert-Eaton myasthenic syndrome (LEMS) is a rare immune-mediated disorder of neuromuscular junctions. The knowledge of the effects of pregnancy on the course of patients with LEMS is limited. Here we describe a patient without a history of previous known illness who has complained of weakness during the last trimester of her pregnancy, delivered a healthy baby and was diagnosed with non-paraneoplastic LEMS during the postpartum period. With this case we wanted to emphasize the effects of pregnancy on the course of patients with LEMS.
Genetics and criminal responsibility.
Trends in cognitive sciences, 2011

Some believe that genetics threatens privacy and autonomy and will eviscerate the concept of human nature. Despite the astonishing research advances, however, none of these dire predictions and no radical transformation of the law have occurred. Advocates have tried to use genetic evidence to affect judgments of criminal responsibility. At present, however genetic research can provide little aid to assessments of criminal responsibility and it does not suggest a radical critique of responsibility.
Musculotopic organization of the motor neurons supplying forelimb and shoulder girdle muscles in the mouse.
Brain structure & function, 2013

We identified the motor neurons (MNs) supplying the shoulder girdle and forelimb muscles in the C57BL/6J mouse spinal cord using Fluoro-Gold retrograde tracer injections. In spinal cord transverse sections from C2 to T2, we observed two MN columns (medial and lateral) both with ventral and dorsal subdivisions. The dorsolateral column consisted of the biceps brachii, forearm extensors, forearm flexors, and hand MNs, and the ventrolateral column consisted of the latissimus dorsi, trapezius, teres major, deltoid, and triceps MNs. The supraspinatus muscle MNs were located in the dorsomedial column, and pectoralis major and serratus anterior MNs were located in the ventromedial columns. MNs of the dorsolateral column innervated the biceps brachii in mid-C4 to mid-C7, forearm extensors in caudal C4 to mid-T1, forearm flexors in rostral C5 to mid-T1, and hand muscles in mid-C8 to mid-T2 segments. The MNs innervating the trapezius were located in mid-C2 to mid-C4, triceps brachii in mid-C6 to rostral T1, deltoid in rostral C4 to mid-C6, teres major in rostral C5 to mid-C8, and latissimus dorsi in mid-C5 to caudal C8. In addition, MNs innervating the supraspinatus were located from rostral C4 to caudal C8, pectoralis major in mid-C6 to mid-T2, and serratus anterior in rostral C5 to caudal C7/rostral C8 segments. While the musculotopic pattern of MN groups was very similar to that documented for other species, we found differences in the position and cranio-caudal extent of some MN pools compared with previous reports. The identification of mouse forelimb MNs can serve as an anatomical reference for studying degenerative MN diseases, spinal cord injury, and developmental gene expression.
Middle infratemporal fossa less invasive approach for radical resection of parapharyngeal tumors: surgical microanatomy and clinical application.
Neurosurgical review, 2016

Surgery of the infratemporal fossa (ITF) and parapharyngeal area presents a formidable challenge to the surgeon due to its anatomical complexity and limited access. Conventional surgical approaches to these regions were often too invasive and necessitate sacrifice of normal function and anatomy. To describe a less invasive transcranial extradural approach to ITF parapharyngeal lesions and to determine its advantages, 17 patients with ITF parapharyngeal neoplasms who underwent tumor resection via this approach were enrolled in the study. All lesions located in the ITF precarotid parapharyngeal space were resected through a small operative corridor between the trigeminal nerve third branch (V3) and the temporomandibular joint (TMJ). Surgical outcomes and postoperative complications were evaluated. Pathological diagnosis included schwannoma in eight cases, paraganglioma in two cases, gangliocytoma in two cases, carcinosarcoma in one case, giant cell tumor in one case, pleomorphic adenoma in one case, chondroblastoma in one case, and juvenile angiofibroma in one case. Gross total resection was achieved in 12 cases, near-total and subtotal resection were in 3 and 2 cases, respectively. The most common postoperative complication was dysphagia. Surgical exposure can be customized from minimal (drilling of retrotrigeminal area) to maximal (full skeletonization of V3, removal of all structures lying lateral to the petrous segment of internal carotid artery) according to tumor size and location. Since the space between the V3 and TMJ is the main corridor of this approach, the key maneuver is the anterior translocation of V3 to obtain an acceptable surgical field.
Noninvasive prediction of shunt operation outcome in idiopathic normal pressure hydrocephalus.
Scientific reports, 2015

Idiopathic normal pressure hydrocephalus (iNPH) is a syndrome characterized by gait disturbance, cognitive deterioration and urinary incontinence in elderly individuals. These symptoms can be improved by shunt operation in some but not all patients. Therefore, discovering predictive factors for the surgical outcome is of great clinical importance. We used normalized power variance (NPV) of electroencephalography (EEG) waves, a sensitive measure of the instability of cortical electrical activity, and found significantly higher NPV in beta frequency band at the right fronto-temporo-occipital electrodes (Fp2, T4 and O2) in shunt responders compared to non-responders. By utilizing these differences, we were able to correctly identify responders and non-responders to shunt operation with a positive predictive value of 80% and a negative predictive value of 88%. Our findings indicate that NPV can be useful in noninvasively predicting the clinical outcome of shunt operation in patients with iNPH.
A single nucleotide polymorphism in the human serotonin transporter introduces a new site for N-linked glycosylation.
Neuropharmacology, 2009

The human serotonin transporter (hSERT) is responsible for reuptake of serotonin (5-HT) from the synaptic cleft and is target for antidepressant medicine. Differential hSERT activity caused by genetic polymorphisms is believed to affect the risk of developing depression and, moreover, to affect the response to antidepressant therapy. The hSERT contains in the second extracellular loop (EL2) two sites for N-linked glycosylation that are critical for functional transporter expression. Here we examine a non-synonymous single nucleotide polymorphism (SNP) in EL2 that gives rise to a potential third glycosylation site due to substitution of a lysine at position 201 with an asparagine (K201N). In agreement with introduction of an additional glycosylation site, western blot analysis showed migration of hSERT K201N corresponding to a higher molecular weight than wild type hSERT upon expression in both HEK293 cells and primary cultures of cortical neurons. An increase in molecular weight was not observed after removal of glycans with peptide N-glycosidase F (PNGase F). Quantitative analysis of western blots indicated significantly increased total transporter expression ( approximately 30%) for hSERT K201N as compared to hSERT in both cell systems. The increase in expression was accompanied by corresponding significant increases in the number of [(3)H]citalopram binding sites and in the V(max) for [(3)H]5-HT uptake. Characterization of mutants carrying all possible combinations of glycosylation sites demonstrated clear correlation between the number of glycosylation sites and the level of transporter activity, and showed that K201N could substitute for either one of the two original glycosylation sites.
Stress-Related Immune Markers in Depression: Implications for Treatment.
The international journal of neuropsychopharmacology, 2016

Major depression is a serious psychiatric disorder; however, the precise biological basis of depression still remains elusive. A large body of evidence implicates a dysregulated endocrine and inflammatory response system in the pathogenesis of depression. Despite this, given the heterogeneity of depression, not all depressed patients exhibit dysregulation of the inflammatory and endocrine systems. Evidence suggests that inflammation is associated with depression in certain subgroups of patients and that those who have experienced stressful life events such as childhood trauma or bereavement may be at greater risk of developing depression. Consequently, prolonged exposure to stress is thought to be a key trigger for the onset of a depressive episode. This review assesses the relationship between stress and the immune system, with a particular interest in the mechanisms by which stress impacts immune function, and how altered immune functioning, in turn, may lead to a feed forward cascade of multiple systems dysregulation and the subsequent manifestation of depressive symptomology. The identification of stress-related immune markers and potential avenues for advances in therapeutic intervention is vital. Changes in specific biological markers may be used to characterize or differentiate depressive subtypes or specific symptoms and may predict treatment response, in turn facilitating a more effective, targeted, and fast-acting approach to treatment.