Humans rely heavily on facial expressions for social communication to convey their thoughts and emotions and to understand them in others. One prominent but controversial view is that humans learn to recognize the significance of facial expressions by mimicking the expressions of others. This view predicts that an inability to make facial expressions (e.g., facial paralysis) would result in reduced perceptual sensitivity to others' facial expressions. To test this hypothesis, we developed a diverse battery of sensitive emotion recognition tasks to characterize expression perception in individuals with Moebius Syndrome (MBS), a congenital neurological disorder that causes facial palsy. Using computer-based detection tasks we systematically assessed expression perception thresholds for static and dynamic face and body expressions. We found that while MBS individuals were able to perform challenging perceptual control tasks and body expression tasks, they were less efficient at extracting emotion from facial expressions, compared to matched controls. Exploratory analyses of fMRI data from a small group of MBS participants suggested potentially reduced engagement of the amygdala in MBS participants during expression processing relative to matched controls. Collectively, these results suggest a role for facial mimicry and consequent facial feedback and motor experience in the perception of others' facial expressions.
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http://dx.doi.org/10.1016/j.cortex.2023.08.014 | DOI Listing |
J Neurol
January 2025
Department of Neurology and Neurosciences, Donostia University Hospital, Biogipuzkoa Health Research Institute, Donostia-San Sebastián, Spain.
Background: Alpha-actinin-2, a protein with high expression in cardiac and skeletal muscle, is located in the Z-disc and plays a key role in sarcomere stability. Mutations in ACTN2 have been associated with both hypertrophic and dilated cardiomyopathy and, more recently, with skeletal myopathy.
Methods: Genetic, clinical, and muscle imaging data were collected from 37 patients with an autosomal dominant ACTN2 myopathy belonging to 11 families from Spain and Belgium.
J Neurol
January 2025
Laboratory of Clinical Pharmacology and Therapeutics, Faculdade de Medicina, Universidade de Lisboa, Av. Prof. Egas Moniz, 1649-028, Lisbon, Portugal.
Background: Drooling, defined as the unintentional loss of saliva from the anterior oral cavity, remains poorly understood in terms of the underlying clinical factors in people with Parkinson's disease (PwP). This study aims to clarify these factors by analyzing predictors and secondarily the correlates with the severity of drooling in PwP.
Methods: We conducted a cross-sectional study involving 42 PwP with drooling and 59 without drooling.
J Rehabil Assist Technol Eng
January 2025
University of Regina, Regina, SK, Canada.
Regular use of standardized observational tools to assess nonverbal pain behaviors results in improved pain care for older adults with severe dementia. While frequent monitoring of pain behaviors in long-term care (LTC) is constrained by resource limitations, computer vision technology has the potential to mitigate these challenges. A computerized algorithm designed to assess pain behavior in older adults with and without dementia was recently developed and validated using video recordings.
View Article and Find Full Text PDFHead Neck Pathol
January 2025
Department of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Purpose: Recurrent diffuse-type tenosynovial giant cell tumor: Clinical presentation, Diagnosis, and Management.
Background: Tenosynovial giant cell tumor (TGCT), is a neoplasm arising from synovial joints, bursae, or tendon sheaths. The initial clinical symptoms are vague and non-diagnostic.
Mol Biol Rep
January 2025
Institute of Health Sciences, Department of Medical and Surgical Research, Hacettepe University, Ankara, Turkey.
Background: La-related protein 7 (LARP7) is a key regulator of RNA metabolism and is thought to play a role in various cellular processes. LARP7 gene autosomal recessive mutations are the cause of Alazami syndrome, which presents with skeletal abnormalities, intellectual disabilities, and facial dysmorphisms. This study aimed to determine the role of LARP7 in modulating gene expression dynamics during osteogenesis.
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