Time perception

About: Time perception is a research topic. Over the lifetime, 1918 publications have been published within this topic receiving 87020 citations.

Testing Some Implications of the Sensory Physiological Model of the Time Sense

Abstract: Summary. In this paper some implications of the pulse generator model of time perception have been tested. In the case of serial (re)production of an interval a lengthening effect occurs. Generally, this phenomenon is explained by assuming that the time-keeper is driven by the state of general physiological activation which decreases in the course of the task. An experiment was carried out in which EEG activity was recorded during the time estimation process. It appeared that a lengthening effect occurred, but there was no correlation between the reproduction times and the means of the EEG spectra, however. In a second experiment two series of time estimations were compared as a function of administering a placebo and methamphetamine. In the latter case the model predicts that no lengthening will occur since arousal (at least for a short period of time) is kept at a high and constant level. In fact, no differences between the regressions of the time estimation curves before and after drug administration have been found, so that the predictions of the model as regards the origin of lengthening could not be supported. It is suggested that the nature of the effect should be studied within the framework of the cognitive theory of time experience which offers various starting points in this respect.

Temporal binding and internal clocks

Abstract: Temporal binding refers to the perceptual attraction of causally related events, which are perceived as closer together in time than unrelated events. This effect is not only characterised by the perceived attraction of cause and effect, but also by a contraction of the interval separating the events. Since the original article on temporal binding (Haggard, Clarke, & Kalogeras, 2002), research has identified the conditions necessary for the effect to occur. While predictability and contiguity are both necessary, it is causality and not intentional action that is the root of the effect (Buehner, 2012). Despite this fruitful work, little is known about how temporal binding is realised. Event perception approaches suggest that binding arises as a realignment of sensory streams. Time perception approaches, in contrast, suggest that binding arises due to a changes in temporal perception during the interval. Given the precedence for the latter approach in the literature (Humphreys & Buehner, 2009; Wenke & Haggard, 2009), I therefore applied an internal clock model of time perception to temporal binding. In Experiments 1 – 4 (Chapter 3), I explored whether binding is effected by the general slowing of a rate of an internal clock. Participants made verbal estimates of either an interval (in causal and noncausal conditions), or of an unrelated event embedded either before or during the interval. I hypothesised that changes in a general clock rate would both affect intervals and embedded events, such that events embedded during causal intervals would be judged as shorter than those embedded during noncausal intervals. The results revealed that causal trial intervals were judged as shorter than noncausal intervals, while no effect was found for embedded events. These results suggested that binding is effected by clock processes specific to cause-effect intervals. Experiments 5 - 8 (Chapter 4) examined whether binding might arise either due to changes 1 in a specific clock rate or to differential timing latencies. Using a temporal discrimination procedure, participants judged whether a variable duration interval was shorter or longer than a reference interval. The point of subjective equality (PSE) was computed for each reference duration, and then modelled using regression. The results revealed a significant binding effect, but more importantly, significant differences in regression slopes between causal and noncausal conditions in three out of four experiments. These results supported the hypothesis of a slower clock rate in temporal binding. In Experiments 9 - 10 (Chapter 5) I verified the results of Chapter 4 by examining discrimination thresholds between two causal and two noncausal intervals. In both experiments (Chapter 5), higher just-noticeable- difference (JND) thresholds were found in causal conditions, supporting the notion of a slower clock rate in cause-effect intervals. Taken together, the present body of work supports the notion that temporal binding is effected by a slower internal clock rate. Future experiments might investigate whether clock slowing in binding is driven by causality or predictability.

Crossmodal emotional modulation of time perception

Abstract: The thesis that consists of three studies investigated how visual affective stimuli or action as contexts influence crossmodal time processing, particularly on the role of the crossmodal/sensorimotor linkage in time perception. By using different types of emotional stimuli (e.g., threat, disgust, and neutral pictures) and manipulating the possibility of near-body interactions, three studies disassociated the impacts of embodied action from emotional dimensions (arousal and valence) on crossmodal emotional modulation in time perception. The whole thesis thus offered the first behavioral evidence that embodied action is an important factor that expands subjective tactile duration and facilitates tactile selection (modality-specific temporal processing) in emotion and action contexts. Moreover, subjective expansion of duration by threat and action contexts may reflect the evolutionary coupling of our perceptual and motor systems to adapt to the specific environments for survival and success.

How perception of time differs under different situations: Different behaviors of the central nervous system as a complex dynamic system.

Abstract: rent results might be confounded by metbolic abnormalities. Consistent evidence suggests that the diameters of retinal arterioles are inversely proportional to high blood pressure and body mass index (BMI), while diameters of retinal venules are proportional to increase of BMI, serum glucose, triglyceride, and cholesterol levels. We aimed to assess retinal structures, including neural and vascular components, in patients with BD without metabolic problems (see Methods in Appendix S1). Moreover, as neurotrophins, such as vascular endothelial growth factor (VEGF), play important roles for vascular abnormalities in the retina (i.e., excessive levels of VEGF lead to proliferative retinopathy in diabetes mellitus), we also controlled the levels of growth factors. In order to avoid effects from age-related retinal degeneration, we limited the age range for participants to 18–45 years and 6 of myopia or hypermetropia and 3 of astigmatism were the upper limits for exclusion. History of any eye disease or surgery, brain surgery, any systemic disease, vascular or neurological diseases, hypertension, diabetes mellitus, nicotine consumption, anemia, and any infectious or inflammatory disease in the last 3 months were the other exclusion criteria. Accordingly, 31 HC and 41 patients with BD type I were enrolled (Table S1 in Appendix S1). Patients were in remission (n = 14), manic (n = 13), or depressed (n = 14) states. Moreover, patients were in the first 10 years of their disorder. Following psychiatric evaluations (see Methods in Appendix S1), participants had a comprehensive eye examination. Retinal assessments were performed with optical coherence tomography (OCT; Fig. S1A in Appendix S1; Spectralis OCT, Heidelberg, Germany) and a TOPCON-TRC.50IX retinal fundus camera (TOPCON Medical Systems Inc., Oakland, NJ, USA) (Fig. S1B–D in Appendix S1). Both eyes of each participant were photographed with a 50 digital camera with total magnification of 18.4× in a darkened room. All photographs were taken with the optic disk at the center of both eyes. The measured area of retinal vascular parameters was detected in the ring region where located between 0.5 and 1.0 disk diameter, 0.75 disk diameter, from the optic disk margin (see details in the Methods in Appendix S1). Adobe Photoshop CS6 and ImageJ (version 1.52n, Wayne Rasband, National Institute of Health, Bethesda, MD, USA) software were used for the image-analysis process. From a line selection five measurements (selection and two parallel shifts in both directions) were taken. According to the formula, central retinal arterial equivalent (CRAE) and central retinal venular equivalent (CRVE) were calculated. Comparison between groups in terms of biochemical and OCT measurements are reported in Tables S2 and S3 in Appendix S1, respectively. Calibers of retinal vessels (arterioles and venules) did not differ between the BD and HC groups (Table 1). Furthermore, there were no significant differences among manic, depressed, and euthymic BD states. Neurotrophin levels did not differ between the groups (Table S1) but VEGF levels were slightly decreased in the BD group in comparison to the HC group. However, there was no correlation between neurotrophin levels and the retinal measures of the vascular or neural structures (Tables S4 and S5 in Appendix S1). VEGF was the determinant of CRAE/CRVE ratio in patients with BD (Table S6 in Appendix S1). Disease progression, diabetes, hypertension, obesity and smoking may cause microvascular changes in the retina and most of the studies in the literature have not taken these risk factors into account. We could not detect retinal vascular abnormality in patients with BD. Obesity, increased insulin resistance, dyslipidemia, metabolic syndrome, and hypertension are risk factors for adverse vascular outcomes by severely disrupting endothelial functions as a result of local inflammation and oxidative damage. Moreover, it has been suggested that vascular pathologies cannot be fully explained by the above-mentioned risk factors in BD. Future studies controlling for the risk factors should further investigate vascular disturbances in BD.