scholarly journals Visual adaptation and 7T fMRI reveal facial identity processing in the human brain under shallow interocular suppression

NeuroImage ◽  
2021 ◽  
pp. 118622
Author(s):  
Runnan Cao ◽  
Chencan Qian ◽  
Shiwen Ren ◽  
Zhifen He ◽  
Sheng He ◽  
...  
2015 ◽  
Vol 15 (12) ◽  
pp. 165
Author(s):  
Marlena Itz ◽  
Jessika Golle ◽  
Stefanie Luttmann ◽  
Stefan Schweinberger ◽  
Jürgen Kaufmann

2021 ◽  
Author(s):  
◽  
Lauren Clare Bell

<p>Individuals with developmental prosopagnosia experience lifelong deficits recognising facial identity, but whether their ability to process facial expression is also impaired is unclear. Addressing this issue is key for understanding the core deficit in developmental prosopagnosia, and for advancing knowledge about the mechanisms and development of normal face processing. In this thesis, I report two online studies on facial expression processing with large samples of prosopagnosics. In Study 1, I compared facial expression and facial identity perception in 124 prosopagnosics and 133 controls. I used three perceptual tasks including simultaneous matching, sequential matching, and sorting. I also measured inversion effects to examine whether prosopagnosics rely on typical face mechanisms. Prosopagnosics showed subtle deficits with facial expression, but they performed worse with facial identity. Prosopagnosics also showed reduced inversion effects for facial identity but normal inversion effects for facial expression, suggesting they use atypical mechanisms for facial identity but normal mechanisms for facial expression. In Study 2, I extended the findings of Study 1 by assessing facial expression recognition in 78 prosopagnosics and 138 controls. I used four labelling tasks that varied on whether the facial expressions were basic (e.g., happy) or complex (e.g., elated), and whether they were displayed via static (i.e., images) or dynamic (i.e., video clips) stimuli. Prosopagnosics showed subtle deficits with basic expressions but performed normally with complex expressions. Further, prosopagnosics did not show reduced inversion effects for both types of expressions, suggesting they use similar recognition mechanisms as controls. Critically, the subtle expression deficits that prosopagnosics showed in both studies can be accounted for by autism traits, suggesting that expression deficits are not a feature of prosopagnosia per se. I also provide estimates of the prevalence of deficits in facial expression perception (7.70%) and recognition (2.56% - 5.13%) in prosopagnosia, both of which suggest that facial expression processing is normal in the majority of prosopagnosics. Overall, my thesis demonstrates that facial expression processing is not impaired in developmental prosopagnosia, and suggests that facial expression and facial identity processing rely on separate mechanisms that dissociate in development.</p>


2016 ◽  
Vol 108 (2) ◽  
pp. 369-396 ◽  
Author(s):  
Marlena L. Itz ◽  
Jessika Golle ◽  
Stefanie Luttmann ◽  
Stefan R. Schweinberger ◽  
Jürgen M. Kaufmann

2017 ◽  
Vol 17 (10) ◽  
pp. 1262
Author(s):  
Dan Nemrodov ◽  
Matthias Niemeier ◽  
Ashutosh Patel ◽  
Adrian Nestor

2021 ◽  
Author(s):  
◽  
Lauren Clare Bell

<p>Individuals with developmental prosopagnosia experience lifelong deficits recognising facial identity, but whether their ability to process facial expression is also impaired is unclear. Addressing this issue is key for understanding the core deficit in developmental prosopagnosia, and for advancing knowledge about the mechanisms and development of normal face processing. In this thesis, I report two online studies on facial expression processing with large samples of prosopagnosics. In Study 1, I compared facial expression and facial identity perception in 124 prosopagnosics and 133 controls. I used three perceptual tasks including simultaneous matching, sequential matching, and sorting. I also measured inversion effects to examine whether prosopagnosics rely on typical face mechanisms. Prosopagnosics showed subtle deficits with facial expression, but they performed worse with facial identity. Prosopagnosics also showed reduced inversion effects for facial identity but normal inversion effects for facial expression, suggesting they use atypical mechanisms for facial identity but normal mechanisms for facial expression. In Study 2, I extended the findings of Study 1 by assessing facial expression recognition in 78 prosopagnosics and 138 controls. I used four labelling tasks that varied on whether the facial expressions were basic (e.g., happy) or complex (e.g., elated), and whether they were displayed via static (i.e., images) or dynamic (i.e., video clips) stimuli. Prosopagnosics showed subtle deficits with basic expressions but performed normally with complex expressions. Further, prosopagnosics did not show reduced inversion effects for both types of expressions, suggesting they use similar recognition mechanisms as controls. Critically, the subtle expression deficits that prosopagnosics showed in both studies can be accounted for by autism traits, suggesting that expression deficits are not a feature of prosopagnosia per se. I also provide estimates of the prevalence of deficits in facial expression perception (7.70%) and recognition (2.56% - 5.13%) in prosopagnosia, both of which suggest that facial expression processing is normal in the majority of prosopagnosics. Overall, my thesis demonstrates that facial expression processing is not impaired in developmental prosopagnosia, and suggests that facial expression and facial identity processing rely on separate mechanisms that dissociate in development.</p>


2012 ◽  
Vol 42 (9) ◽  
pp. 1913-1924 ◽  
Author(s):  
M. T. Keener ◽  
J. C. Fournier ◽  
B. C. Mullin ◽  
D. Kronhaus ◽  
S. B. Perlman ◽  
...  

BackgroundIndividuals with bipolar disorder demonstrate abnormal social function. Neuroimaging studies in bipolar disorder have shown functional abnormalities in neural circuitry supporting face emotion processing, but have not examined face identity processing, a key component of social function. We aimed to elucidate functional abnormalities in neural circuitry supporting face emotion and face identity processing in bipolar disorder.MethodTwenty-seven individuals with bipolar disorder I currently euthymic and 27 healthy controls participated in an implicit face processing, block-design paradigm. Participants labeled color flashes that were superimposed on dynamically changing background faces comprising morphs either from neutral to prototypical emotion (happy, sad, angry and fearful) or from one identity to another identity depicting a neutral face. Whole-brain and amygdala region-of-interest (ROI) activities were compared between groups.ResultsThere was no significant between-group difference looking across both emerging face emotion and identity. During processing of all emerging emotions, euthymic individuals with bipolar disorder showed significantly greater amygdala activity. During facial identity and also happy face processing, euthymic individuals with bipolar disorder showed significantly greater amygdala and medial prefrontal cortical activity compared with controls.ConclusionsThis is the first study to examine neural circuitry supporting face identity and face emotion processing in bipolar disorder. Our findings of abnormally elevated activity in amygdala and medial prefrontal cortex (mPFC) during face identity and happy face emotion processing suggest functional abnormalities in key regions previously implicated in social processing. This may be of future importance toward examining the abnormal self-related processing, grandiosity and social dysfunction seen in bipolar disorder.


eNeuro ◽  
2018 ◽  
Vol 5 (1) ◽  
pp. ENEURO.0358-17.2018 ◽  
Author(s):  
Dan Nemrodov ◽  
Matthias Niemeier ◽  
Ashutosh Patel ◽  
Adrian Nestor

2010 ◽  
Vol 68 ◽  
pp. e409-e410
Author(s):  
Hirokazu Doi ◽  
Akiko Arimura ◽  
Emiko Hirase ◽  
Wakiko Kitamura ◽  
Kazuyuki Shinohara

2014 ◽  
Vol 27 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Kazumichi Matsumiya

The face aftereffect (FAE; the illusion of faces after adaptation to a face) has been reported to occur without retinal overlap between adaptor and test, but recent studies revealed that the FAE is not constant across all test locations, which suggests that the FAE is also retinotopic. However, it remains unclear whether the characteristic of the retinotopy of the FAE for one facial aspect is the same as that of the FAE for another facial aspect. In the research reported here, an examination of the retinotopy of the FAE for facial expression indicated that the facial expression aftereffect occurs without retinal overlap between adaptor and test, and depends on the retinal distance between them. Furthermore, the results indicate that, although dependence of the FAE on adaptation-test distance is similar between facial expression and facial identity, the FAE for facial identity is larger than that for facial expression when a test face is presented in the opposite hemifield. On the basis of these results, I discuss adaptation mechanisms underlying facial expression processing and facial identity processing for the retinotopy of the FAE.


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