Emotion dysregulation in borderline personality disorder (BPD) is associated with loss of cognitive control in the face of intense negative emotion. Negative emotional context may interfere with cognitive processing through the dysmodulation of brain regions involved in regulation of emotion, impulse control, executive function and memory. Structural and metabolic brain abnormalities have been reported in these regions in BPD. Using novel fMRI protocols, we investigated the neural basis of negative affective interference with cognitive processing targeting these regions. Attention-driven Go No-Go and X-CPT (continuous performance test) protocols, using positive, negative and neutral Ekman faces, targeted the orbital frontal cortex (OFC) and the anterior cingulate cortex (ACC), respectively. A stimulus-driven Episodic Memory task, using images from the International Affective Pictures System, targeted the hippocampus (HIP). Participants comprised 23 women with BPD, who were compared with 15 healthy controls. When Negative>Positive faces were compared in the Go No-Go task, BPD subjects had hyper-activation relative to controls in areas reflecting task-relevant processing: the superior parietal/precuneus and the basal ganglia. Decreased activation was also noted in the OFC, and increased activation in the amygdala (AMY). In the X-CPT, BPD subjects again showed hyper-activation in task-relevant areas: the superior parietal/precuneus and the ACC. In the stimulus-driven Episodic Memory task, BPD subjects had decreased activation relative to controls in the HIP, ACC, superior parietal/precuneus, and dorsal prefrontal cortex (dPFC) (for encoding), and the ACC, dPFC, and HIP for retrieval of Negative>Positive pictures, reflecting impairment of task-relevant functions. Negative affective interference with cognitive processing in BPD differs from that in healthy controls and is associated with functional abnormalities in brain networks reported to have structural or metabolic abnormalities. Task demands exert a differential effect on the cognitive response to negative emotion in BPD compared with control subjects.
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http://dx.doi.org/10.1016/j.pscychresns.2015.04.006 | DOI Listing |
Am J Geriatr Psychiatry
December 2024
HM CINAC (Centro Integral de Neurociencias Abarca Campal) (RFF, CDTP, CGS), Hospital Universitario HM Puerta del Sur, HM Hospitales. Madrid, Spain; Instituto de Investigación Sanitaria HM Hospitales (RFF, CDTP, CGS), Madrid, Spain; Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED) (CGS), Instituto Carlos III, Madrid, Spain; University CEU-San Pablo (CGS), Madrid, Spain. Electronic address:
Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor and non-motor manifestations, including alexithymia. This condition is defined by difficulty in recognizing, articulating, and expressing one's emotional states. In this study, we conducted a systematic review and meta-analysis to compare the prevalence of alexithymia in PD patients and a healthy population, and to identify associated demographic and clinical factors.
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December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK; Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany. Electronic address:
Background: A preference for sooner-smaller over later-larger rewards, known as delay discounting, is a candidate transdiagnostic marker of waiting impulsivity and a research domain criterion. While abnormal discounting rates have been associated with many psychiatric diagnoses and abnormal brain structure, the underlying neuropsychological processes remain largely unknown. Here, we deconstruct delay discounting into choice and rate processes by testing different computational models and investigate their associations with white matter tracts.
View Article and Find Full Text PDFNeurosci Lett
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Neurobiology Unit, Institute for Biotechnology and Biomedicine (BIOTECMED), University of Valencia, Spain. Electronic address:
Neuronal structural plasticity gives the adult brain the capacity to adapt to internal or external factors by structural and molecular changes. These plastic processes seem to be mediated, among others, by the action of the neurotransmitter serotonin through specific receptors (5-HTRs). Previous studies have shown that the maturation of granule cells in the hippocampus is mediated by 5-HT3.
View Article and Find Full Text PDFJ Biol Chem
December 2024
Department of Pharmacology, Addiction Science, and Toxicology, College of Medicine, The University of Tennessee Health Science Center; Memphis, 38163. Electronic address:
Familial Alzheimer's disease (FAD) is frequently associated with mutations in the amyloid precursor protein (APP), which are thought to lead to cognitive deficits by impairing NMDA receptor (NMDAR)-dependent forms of synaptic plasticity. Given the reliance of synaptic plasticity on NMDAR-mediated Ca entry, shaping of NMDAR activity by APP and/or its disease-causing variants could provide a basis for understanding synaptic plasticity impairments associated with FAD. A region of APP (residues 639-644 within APP695) processed by the γ-secretase complex, which generates amyloid β (Aβ) peptides, is a hotspot for FAD mutations.
View Article and Find Full Text PDFAsian J Psychiatr
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Centre of Disease Control and Prevention Department, Hamad Medical Corporation, Qatar.
Child and adolescent mental health disorders in Qatar remain significantly underserved due to a critical shortage of specialists, stigma, and logistical barriers. This paper proposes implementing a Collaborative Care Model (CoCM) within Qatar's primary care settings, leveraging existing infrastructure, such as the CERNER electronic health record system, and innovations like telepsychiatry and AI-driven tools. The model integrates task-sharing among interdisciplinary teams to enhance accessibility and continuity of care.
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