Psychology moved beyond the stimulus response mapping of behaviorism by adopting an information processing framework. This shift from behavioral to cognitive science was partly inspired by work demonstrating that the concept of information could be defined and quantified (Shannon, 1948). This transition developed further from cognitive science into cognitive neuroscience, in an attempt to measure information in the brain. In the cognitive neurosciences, however, the term information is often used without a clear definition. This paper will argue that, if the formulation proposed by Shannon is applied to modern neuroimaging, then numerous results would be interpreted differently. More specifically, we argue that much modern cognitive neuroscience implicitly focuses on the question of how we can interpret the activations we record in the brain (experimenter-as-receiver), rather than on the core question of how the rest of the brain can interpret those activations (cortex-as-receiver). A clearer focus on whether activations recorded via neuroimaging can actually act as information in the brain would not only change how findings are interpreted but should also change the direction of empirical research in cognitive neuroscience.
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http://dx.doi.org/10.3758/s13423-016-1002-0 | DOI Listing |
Eur Child Adolesc Psychiatry
January 2025
Department of Child and Adolescent Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
While impaired response inhibition has been reported in attention-deficit/hyperactivity disorder (ADHD), findings in disruptive behavior disorders (DBDs) have been inconsistent, probably due to unaccounted effects of co-occurring ADHD in DBD. This study investigated the associations of behavioral and neural correlates of response inhibition with DBD and ADHD symptom severity, covarying for each other in a dimensional approach. Functional magnetic resonance imaging data were available for 35 children and adolescents with DBDs (8-18 years old, 19 males), and 31 age-matched unaffected controls (18 males) while performing a performance-adjusted stop-signal task.
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January 2025
Department of Internal Medicine, General Hospital Oberndorf, Teaching Hospital of the Paracelsus Medical University, Salzburg, Austria.
Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by systemic inflammation. While RA primarily affects the joints, its systemic effects may lead to an increased cerebro- and cardiovascular risk. Atherosclerosis of the carotid arteries is a significant risk factor for cerebrovascular events and serves as a surrogate marker for cardiovascular risk.
View Article and Find Full Text PDFAust N Z J Psychiatry
January 2025
Neuropsychiatry Centre, The Royal Melbourne Hospital, Parkville, VIC, Australia.
Introduction: Young-onset neurocognitive symptoms result from a heterogeneous group of neurological and psychiatric disorders which present a diagnostic challenge. To identify such factors, we analysed the Biomarkers in Younger-Onset Neurocognitive Disorders cohort, a study of individuals <65 years old presenting with neurocognitive symptoms for a diagnosis and who have undergone cognitive and biomarker analyses.
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J Headache Pain
January 2025
Department of Neurology, The David Geffen School of Medicine at UCLA, Los Angeles, USA.
Background: Migraine progression, particularly from episodic to chronic migraine (CM), increases disease burden and healthcare costs. Understanding the new concept of "Medication Underuse Headache" should encourage the health care provider to consider early intervention with calcitonin gene-related peptide (CGRP) monoclonal antibodies. Galcanezumab given early in the course of the disease, may prevent migraine chronification and have a robust response, moreso than when initiated in later stages of migraine.
View Article and Find Full Text PDFNat Med
January 2025
Huntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease with the age at which characteristic symptoms manifest strongly influenced by inherited HTT CAG length. Somatic CAG expansion occurs throughout life and understanding the impact of somatic expansion on neurodegeneration is key to developing therapeutic targets. In 57 HD gene expanded (HDGE) individuals, ~23 years before their predicted clinical motor diagnosis, no significant decline in clinical, cognitive or neuropsychiatric function was observed over 4.
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