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Limb apraxia is a cognitive-motor disorder typically resulting from left hemisphere stroke, characterized by an inability to perform skilled limb movements despite intact motor and sensory functions. Previous studies suggest that individuals with apraxia exhibit deficits in sensorimotor integration, particularly in detecting temporal discrepancies between movement and sensory feedback. However, whether these deficits affect explicit sense of agency (SoA) remains unclear. This study investigated the time window for sensorimotor integration and explicit SoA in post-stroke patients with and without apraxia. Twenty patients with left hemisphere stroke participated in a delay detection task assessing sensory-sensory and sensorimotor integration and an agency attribution task measuring explicit SoA. The results demonstrated that apraxic patients had a significantly prolonged delay detection threshold and reduced steepness in the active movement condition, indicating an altered time window for sensorimotor integration. In contrast, there were no significant differences between apraxic and non-apraxic patients in the time window for explicit SoA. These findings suggest that while apraxic patients exhibit deficits in sensorimotor integration, their explicit SoA remains preserved. This dissociation supports the notion that explicit SoA may be maintained through compensatory cognitive processes despite impairments at the sensorimotor level. Further research is needed, considering the limitations of this study, to achieve a more comprehensive understanding of SoA in apraxia.

BackgroundSense of agency (SoA) refers to the subjective feeling that one is the agent who causes and controls one’s own actions and those effects on the external world. It’s widely known that patients with schizophrenia show aberrant SoA, but its cognitive and neural mechanisms remain unclear. Previous studies suggest that abnormal SoA is probably due to impaired predictive processes, such as predicting sensory feedbacks according to one’s own motor intention or motor commands. However, dysfunction of the prediction process alone cannot explain various symptoms of schizophrenia. The impairment in postdictive processes in patients with schizophrenia is also considered to be important to explain their symptoms. However, how the predictive and postdictive processes actually contribute to the judgment of agency in patients with schizophrenia remains unknown. In the present study, we focus on the functional contribution of the two processes at sensorimotor level to the judgment of agency at the cognitive level, rather than the performance of these functions. Our approach allows us to evaluate the weightings of each contribution quantitatively, and to associate such weightings to symptoms for each individual. The results of our study point to potential useful diagnosis, and can provide important knowledge for treatment in future research.MethodsWe use two sensorimotor tasks (i.e. the reaching task and the control detection task) and one explicit agency judgment task in this study. In all tasks, participants move one or several dots on a screen by moving a mouse. The speed of the dots’ motion always corresponds to participants’ mouse movement, but the direction of the dots’ motion is combined with both participants’ motion and prerecorded motion, and is applied with a certain angular bias. In the reaching task, participants move the dot to touch a destination on screen as quickly as possible. This task is designed to measure the extent of prediction errors at the sensorimotor level, which is considered as an important signal for the predictive process underlying agency judgment. In the control detection task, participants move three dots simultaneously, and identified one dot that can be partially controlled by their mouse movement, while the other two dots move in pre-recorded directions. This task does not require explicit judgment of agency. It measures the postdictive process that to detect the regularity between the visual feedbacks and one’s own movements at the sensorimotor level. At last, in the explicit agency judgment task, participants made binary judgment (i.e. yes or no) regarding whether they feel that they controlled the moving direction of the dot or not in each condition. In summary, the two sensorimotor tasks measure the output of predictive and postdictive processes at the sensorimotor level, respectively, and the explicit agency judgment task measures agency judgment at the cognitive level. We designed six experimental conditions, in which the actual angular error and regularity were systematically manipulate. Such manipulation creates variability in the performance of each task, and allows us to use structure equation modelling to analyze the contributions of the performance in the two sensorimotor tasks to the explicit agency judgment task, and to compare the results with healthy controls. We focus on the functional structure of the sensorimotor sub-component and the cognitive judgment of SoA.ResultsThe data collection is currently in progress. We plan to finish it by February.DiscussionWe predict weakened contributions from the two sub-components to SoA in patients, compared to healthy control. We plan to link the quantitatively estimated weightings to individual symptoms including both positive and negative symptoms.

Judgment of agency involves the comparison of motor intention and proprioceptive/visual feedback, in addition to a range of cognitive factors. However, few studies have experimentally examined the differences or correlations between delay detection ability and judgment of agency. Thus, the present study investigated the relationship between delay detection ability and agency judgment using the delay detection task and the agency attribution task. Fifty-eight participants performed the delay detection and agency attribution tasks, and the time windows of each measure were analyzed using logistic curve fitting. The results revealed that the time window of judgment of agency was significantly longer than that of delay detection, and there was a slight correlation between the time windows in each task. The results supported a two-step model of agency, suggesting that judgment of agency involved not only comparison of multisensory information but also several cognitive factors. The study firstly revealed the model in psychophysical experiments.

Aberrant sense of agency (SoA, a feeling of control over one’s own actions and their subsequent events) has been considered key to understanding the pathology of schizophrenia. Behavioral studies have demonstrated that a bidirectional (i.e., excessive and diminished) SoA is observed in schizophrenia. Several neurophysiological and theoretical studies have suggested that aberrancy may be due to temporal delays (TDs) in sensory-motor prediction signals. Here, we examined this hypothesis via computational modeling using a recurrent neural network (RNN) expressing the sensory-motor prediction process. The proposed model successfully reproduced the behavioral features of SoA in healthy controls. In addition, simulation of delayed prediction signals reproduced the bidirectional schizophrenia-pattern SoA, whereas three control experiments (random noise addition, TDs in outputs, and TDs in inputs) demonstrated no schizophrenia-pattern SoA. These results support the TD hypothesis and provide a mechanistic understanding of the pathology underlying aberrant SoA in schizophrenia.

Sense of agency refers to the feeling that one's voluntary actions caused external events. Past studies have shown that compression of the subjective temporal interval between actions and external events, called intentional binding, is closely linked to the experience of agency. Current theories postulate that the experience of agency is constructed via predictive and postdictive pathways. One remaining problem is the source of human causality bias; people often make misjudgments on the causality of voluntary actions and external events depending on their rewarding or punishing outcomes. Although human causality bias implies that sense of agency can be modified by post-action information, convincing empirical findings for this issue are lacking. Here, we hypothesized that sense of agency would be modified by affective valences of action outcomes. To examine this issue, we investigated how rewarding and punishing outcomes following voluntary action modulate behavioral measures of agency using intentional binding paradigm and classical conditioning procedures. In the acquisition phase, auditory stimuli were paired with positive, neutral or negative monetary outcomes. Tone-reward associations were evaluated using reaction times and preference ratings. In the experimental session, participants performed a variant of intentional binding task, where participants made timing judgments for onsets of actions and sensory outcomes while playing simple slot games. Our results showed that temporal binding was modified by affective valences of action outcomes. Specifically, intentional binding was attenuated when negative outcome occurred, consistent with self-serving bias. Our study not only provides evidence for postdictive modification of agency, but also proposes a possible mechanism of human causality bias.

Humans are capable of associating actions with their respective consequences if there is reliable contingency between them. The present study examined the link between the reliability of action consequence and the readiness potential (RP), which is a negative potential observed from about 1–2 s prior to the onset of an action with electroencephalography. In a condition of constant outcome, the participants’ voluntary action always triggered beep sounds; thus, they were able to perceive the contingency between their action and the sound. In contrast, in a condition of inconstant outcome, the participants’ actions only triggered the sound in half the trials. We found that both the early and late RPs were larger in the condition of constant compared to the condition of inconstant outcome. Our results showed that the RPs preceding the voluntary action reflected the reliability of action consequence. In other words, the action-effect contingency enhanced neural activities prior to the action.

The sense of agency refers to the feeling of initiating and controlling one’s actions and their resulting effects on the external environment. Previous studies have uncovered behavioral evidence of excessive self-attribution and, conversely, a reduction in the sense of agency in patients with schizophrenia. We hypothesize that this apparent paradox is likely to result from impairment in lower-level processes underlying the sense of agency, combined with a higher-level compensational bias. The present study employed three behavioral tasks utilizing the same stimuli and experimental design to systematically evaluate multiple factors that influence the sense of agency, including motor control, sensorimotor processing, and self-attribution. Participants’ real-time mouse movements were combined with prerecorded motions of others in ratios of 30/70, 55/45, or 80/20, with an additional angular bias of either 0° or 90°. Twenty-six patients with schizophrenia and 27 health control volunteers participated in the three tasks. Patients with schizophrenia performed significantly worse in the reaching and control detection tasks than healthy controls. However, their self-attribution in the control judgment task was comparable to that of the healthy controls. Patients with schizophrenia were impaired in motor control components and in the detection of control using sensorimotor information, but their evaluation of agency remained relatively less affected. This underscores the importance of distinguishing between different subcomponents when addressing the abnormal sense of agency in patients with schizophrenia. Subsequent cluster analysis revealed that the combined task performance accurately distinguished between the patients and healthy control participants.

The sense of agency is the attribution of oneself as the cause of one's own actions and their effects. Accurate agency judgments are essential for adaptive behaviors in dynamic environments, especially in conditions of uncertainty. However, it is unclear how agency judgments are made in ambiguous situations where self-agency and non-self-agency are both possible. Agency attribution is thus thought to require higher-order neurocognitive processes that integrate several possibilities. Furthermore, neural activity specific to self-attribution, as compared with non-self-attribution, may reflect higher-order critical operations that contribute to constructions of self-consciousness. Based on these assumptions, the present study focused on agency judgments under ambiguous conditions and examined the neural correlates of this operation with functional magnetic resonance imaging. Participants performed a simple but demanding agency-judgment task, which required them to report on whether they attributed their own action as the cause of a visual stimulus change. The temporal discrepancy between the participant's action and the visual events was adaptively set to be maximally ambiguous for each individual on a trial-by-trial basis. Comparison with results for a control condition revealed that the judgment of agency was associated with activity in lateral temporo-parietal areas, medial frontal areas, the dorsolateral prefrontal area, and frontal operculum/insula regions. However, most of these areas did not differentiate between self- and non-self-attribution. Instead, self-attribution was associated with activity in posterior midline areas, including the precuneus and posterior cingulate cortex. These results suggest that deliberate self-attribution of an external event is principally associated with activity in posterior midline structures, which is imperative for self-consciousness.

Radiation therapy is a useful treatment for tumors and vascular malformations of the central nervous system. Radiation therapy is associated with complications, including leukoencephalopathy, radiation necrosis, vasculopathy, and optic neuropathy. Secondary tumors are also often seen long after radiation therapy. Secondary tumors are often benign tumors, such as hemangiomas and meningiomas, but sometimes malignant gliomas and soft tissue sarcomas emerge. We review the imaging findings of complications that may occur after brain radiation therapy.