Failure to engage the temporoparietal junction/posterior superior temporal sulcus predicts impaired naturalistic social cognition in schizophrenia

Brain ◽  
2021 ◽  
Author(s):  
Gaurav H Patel ◽  
Sophie C Arkin ◽  
Daniel Ruiz-Betancourt ◽  
Fabiola I Plaza ◽  
Safia A Mirza ◽  
...  
Keyword(s):  
Social Cognition ◽  
Visual Motion ◽  
Superior Temporal Sulcus ◽  
Motion Processing ◽  
Temporoparietal Junction ◽  
Social Inference ◽  
Cortical Areas ◽  
Visual Motion Processing ◽  
The Right ◽  
Posterior Superior Temporal Sulcus

Abstract Schizophrenia is associated with marked impairments in social cognition. However, the neural correlates of these deficits remain unclear. Here we use naturalistic stimuli to examine the role of the right temporoparietal junction/posterior superior temporal sulcus (TPJ-pSTS)—an integrative hub for the cortical networks pertinent to the understanding complex social situations—in social inference, a key component of social cognition, in schizophrenia. 27 schizophrenia participants (SzP) and 21 healthy controls watched a clip of the movie “The Good, the Bad, and the Ugly” while high resolution multiband fMRI images were collected. We used inter-subject correlation (ISC) to measure the evoked activity, which we then compared to social cognition as measured by The Awareness of Social Inference Test (TASIT). We also compared between groups the TPJ-pSTS BOLD activity 1) relationship with the motion content in the movie, 2) synchronization with other cortical areas involved in the viewing of the movie, and 3) relationship with the frequency of saccades made during the movie. Activation deficits were greatest in middle TPJ (TPJm) and correlated significantly with impaired TASIT performance across groups. Follow-up analyses of the TPJ-pSTS revealed decreased synchronization with other cortical areas, decreased correlation with the motion content of the movie, and decreased correlation with the saccades made during the movie. The functional impairment of the TPJm, a hub area in the middle of the TPJ-pSTS, predicts deficits in social inference in SzP by disrupting the integration of visual motion processing into the TPJ. This disrupted integration then affects the use of the TPJ to guide saccades during the visual scanning of the movie clip. These findings suggest that the TPJ may be a treatment target for improving deficits in a key component of social cognition in SzP.

scholarly journals Visual motion assists in social cognition

2020 ◽  
Vol 117 (50) ◽  
pp. 32165-32168
Author(s):  
Arvid Guterstam ◽  
Michael S. A. Graziano
Keyword(s):  
Social Cognition ◽  
Visual Motion ◽  
Cognitive Model ◽  
Object Motion ◽  
Motion Processing ◽  
Attentional State ◽  
Motion Direction ◽  
Motion Signal ◽  
Visual Motion Processing ◽  
The Brain

Recent evidence suggests a link between visual motion processing and social cognition. When person A watches person B, the brain of A apparently generates a fictitious, subthreshold motion signal streaming from B to the object of B’s attention. These previous studies, being correlative, were unable to establish any functional role for the false motion signals. Here, we directly tested whether subthreshold motion processing plays a role in judging the attention of others. We asked, if we contaminate people’s visual input with a subthreshold motion signal streaming from an agent to an object, can we manipulate people’s judgments about that agent’s attention? Participants viewed a display including faces, objects, and a subthreshold motion hidden in the background. Participants’ judgments of the attentional state of the faces was significantly altered by the hidden motion signal. Faces from which subthreshold motion was streaming toward an object were judged as paying more attention to the object. Control experiments showed the effect was specific to the agent-to-object motion direction and to judging attention, not action or spatial orientation. These results suggest that when the brain models other minds, it uses a subthreshold motion signal, streaming from an individual to an object, to help represent attentional state. This type of social-cognitive model, tapping perceptual mechanisms that evolved to process physical events in the real world, may help to explain the extraordinary cultural persistence of beliefs in mind processes having physical manifestation. These findings, therefore, may have larger implications for human psychology and cultural belief.

Directional pursuit deficits following lesions of the foveal representation within the superior temporal sulcus of the macaque monkey

1987 ◽  
Vol 57 (5) ◽  
pp. 1262-1287 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz ◽  
W. T. Newsome
Keyword(s):  
Visual Field ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Macaque Monkey ◽  
Superior Temporal Sulcus ◽  
Target Motion ◽  
Motion Processing ◽  
Position Information ◽  
Field Representation ◽  
Visual Motion Processing

Ibotenic acid lesions of the middle temporal visual area (MT) have previously been shown to impair a monkey's ability to initiate smooth pursuit eye movements to targets moving in the extrafoveal visual field (30). This is a retinotopic deficit: pursuit is impaired in all directions within the affected portion of the contralateral visual field. In the present experiments we analyzed the effects of lesions of the foveal representation of MT on the maintenance of foveal pursuit. Injections of ibotenic acid were directed toward the representation of the fovea within MT but spread into extrafoveal regions of MT and adjacent visual areas within the superior temporal sulcus. Chemical lesions of the foveal representation produced a directional deficit in the maintenance of pursuit: the monkey failed to match eye speed to target speed when pursuing a target that moved toward the side of the brain with the lesion. This deficit was evident regardless of the part of the visual field in which target motion began, and pursuit at higher target speeds was more severely affected. The directional deficit was qualitatively similar to pursuit deficits observed in human patients following large parietal-occipital lesions. Extension of the lesions into extrafoveal regions of the contralateral visual field representation also resulted in retinotopic deficits for pursuit initiation: the monkey was unable to match the speed of its pursuit eye movement to that of a target or to adjust the amplitude of its saccade to compensate for target motion. The errors in pursuit speed and saccade amplitude for initiation of pursuit into the contralateral visual field were linearly related, which supports the hypothesis that both deficits arise from damage to the same underlying visual motion processing mechanism. The selectivity of the retinotopic deficit for motion information was also investigated by reducing retinal motion through the use of a stabilized image. After the lesion, the monkeys continued normal pursuit when a position error was present during stabilization, supporting the view that the deficit was related to loss of motion but not position information.

Pursuit and optokinetic deficits following chemical lesions of cortical areas MT and MST

1988 ◽  
Vol 60 (3) ◽  
pp. 940-965 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz
Keyword(s):  
Eye Movements ◽  
Visual Field ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Motion Processing ◽  
Temporal Area ◽  
Target Speed ◽  
Pursuit Eye Movements ◽  
Medial Superior Temporal ◽  
Visual Motion Processing

1. Previous experiments have shown that punctate chemical lesions within the middle temporal area (MT) of the superior temporal sulcus (STS) produce deficits in the initiation and maintenance of pursuit eye movements (10, 34). The present experiments were designed to test the effect of such chemical lesions in an area within the STS to which MT projects, the medial superior temporal area (MST). 2. We injected ibotenic acid into localized regions of MST, and we observed two deficits in pursuit eye movements, a retinotopic deficit and a directional deficit. 3. The retinotopic deficit in pursuit initiation was characterized by the monkey's inability to match eye speed to target speed or to adjust the amplitude of the saccade made to acquire the target to compensate for target motion. This deficit was related to the initiation of pursuit to targets moving in any direction in the visual field contralateral to the side of the brain with the lesion. This deficit was similar to the deficit we found following damage to extrafoveal MT except that the affected area of the visual field frequently extended throughout the entire contralateral visual field tested. 4. The directional deficit in pursuit maintenance was characterized by a failure to match eye speed to target speed once the fovea had been brought near the moving target. This deficit occurred only when the target was moving toward the side of the lesion, regardless of whether the target began to move in the ipsilateral or contralateral visual field. There was no deficit in the amplitude of saccades made to acquire the target, or in the amplitude of the catch-up saccades made to compensate for the slowed pursuit. The directional deficit is similar to the one we described previously following chemical lesions of the foveal representation in the STS. 5. Retinotopic deficits resulted from any of our injections in MST. Directional deficits resulted from lesions limited to subregions within MST, particularly lesions that invaded the floor of the STS and the posterior bank of the STS just lateral to MT. Extensive damage to the densely myelinated area of the anterior bank or to the posterior parietal area on the dorsal lip of the anterior bank produced minimal directional deficits. 6. We conclude that damage to visual motion processing in MST underlies the retinotopic pursuit deficit just as it does in MT. MST appears to be a sequential step in visual motion processing that occurs before all of the visual motion information is transmitted to the brainstem areas related to pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

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