Mark C Eldaief1,2,3,4, David L Perez1,2,3,5, Megan Quimby1, Daisy Hochberg1, Alexandra Touroutoglou1,2, Lisa Feldman Barrett2,6,7, Bradford C Dickerson8,9. 1. Frontotemporal Disorders Unit and Alzheimer's Disease Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. 2. Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts, USA. 3. Division of Neuropsychiatry, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. 4. Center for Brain Sciences, Harvard University, Cambridge, Massachusetts, USA. 5. Cognitive Behavioral Neurology Unit, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts, USA. 6. Division of Psychiatric Neuroimaging, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. 7. Department of Psychology, Northeastern University, Boston, Massachusetts, USA. 8. Frontotemporal Disorders Unit and Alzheimer's Disease Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA, brad.dickerson@mgh.harvard.edu. 9. Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts, USA, brad.dickerson@mgh.harvard.edu.
Abstract
BACKGROUND: Although traditionally conceptualized as a language disorder, semantic variant primary progressive aphasia (svPPA) is often accompanied by significant behavioral and affective symptoms which considerably increase disease morbidity. Specifically, these neuropsychiatric symptoms are characterized by breaches in normative socioaffective function, for example, an inability to read social cues, excessive trusting of others, and decreased empathy. Our prior neuroimaging work identified 3 corticolimbic networks anchored in the amygdala, temporal pole, and frontoinsular cortex: an affiliation network, theorized to mediate social approach behavior; an aversion network, theorized to subserve the appraisal of social threat; and a perception network, theorized to mediate the detection of social cues. We hy-pothesized that degeneration of these networks could provide neuroanatomical substrates for socioaffective deficits in svPPA. METHODS: We examined hypothesized relationships between subscores on the Social Impairment Rating Scale (SIRS) and atrophy in each of these 3 networks in a group of 16 svPPA patients (using matched cognitively normal controls as a reference). RESULTS: Consistent with our predictions, the magnitude of atrophy in the affiliation network in svPPA patients correlated with the SIRS subscore of socioemotional detachment, while the magnitude of atrophy in the aversion network in svPPA patients correlated with the SIRS subscore of inappropriate trusting. We did not find the predicted association between perception network atrophy and the SIRS subscore of lack of attention to social cues. CONCLUSION: These findings highlight specific socioaffective deficits in svPPA and provide a neuroanatomical basis for these impairments by linking them to networks commonly targeted in this disorder.
BACKGROUND: Although traditionally conceptualized as a language disorder, semantic variant primary progressive aphasia (svPPA) is often accompanied by significant behavioral and affective symptoms which considerably increase disease morbidity. Specifically, these neuropsychiatric symptoms are characterized by breaches in normative socioaffective function, for example, an inability to read social cues, excessive trusting of others, and decreased empathy. Our prior neuroimaging work identified 3 corticolimbic networks anchored in the amygdala, temporal pole, and frontoinsular cortex: an affiliation network, theorized to mediate social approach behavior; an aversion network, theorized to subserve the appraisal of social threat; and a perception network, theorized to mediate the detection of social cues. We hy-pothesized that degeneration of these networks could provide neuroanatomical substrates for socioaffective deficits in svPPA. METHODS: We examined hypothesized relationships between subscores on the Social Impairment Rating Scale (SIRS) and atrophy in each of these 3 networks in a group of 16 svPPA patients (using matched cognitively normal controls as a reference). RESULTS: Consistent with our predictions, the magnitude of atrophy in the affiliation network in svPPA patients correlated with the SIRS subscore of socioemotional detachment, while the magnitude of atrophy in the aversion network in svPPA patients correlated with the SIRS subscore of inappropriate trusting. We did not find the predicted association between perception network atrophy and the SIRS subscore of lack of attention to social cues. CONCLUSION: These findings highlight specific socioaffective deficits in svPPA and provide a neuroanatomical basis for these impairments by linking them to networks commonly targeted in this disorder.
Authors: Katherine P Rankin; Andrea Salazar; Maria Luisa Gorno-Tempini; Marc Sollberger; Stephen M Wilson; Danijela Pavlic; Christine M Stanley; Shenly Glenn; Michael W Weiner; Bruce L Miller Journal: Neuroimage Date: 2009-06-06 Impact factor: 6.556
Authors: Phillip D Fletcher; Laura E Downey; Hannah L Golden; Camilla N Clark; Catherine F Slattery; Ross W Paterson; Jonathan D Rohrer; Jonathan M Schott; Martin N Rossor; Jason D Warren Journal: Brain Date: 2015-10-12 Impact factor: 13.501
Authors: Charles R Marshall; Chris J D Hardy; Lucy L Russell; Camilla N Clark; Katrina M Dick; Emilie V Brotherhood; Rebecca L Bond; Catherine J Mummery; Jonathan M Schott; Jonathan D Rohrer; James M Kilner; Jason D Warren Journal: Front Neurol Date: 2017-11-16 Impact factor: 4.003