1,987 publications from this institution
ABSTRACT Stochastic differential equations are ubiquitous modeling tools in applied mathematics and the sciences. In most modeling scenarios, random fluctuations driving dynamics or motion have some nontrivial temporal correlation structure, which renders the SDE non‐Markovian; a phenomenon commonly known as ‘colored’’ noise. Thus, an important objective is to develop effective tools for mathematically and numerically studying (possibly non‐Markovian) SDEs. In this paper, we formalize a mathematical theory for analyzing and numerically studying SDEs based on so‐called “generalized coordinates of motion.” Like the theory of rough paths, we analyze SDEs pathwise for any given realization of the noise, not solely probabilistically. Like the established theory of Markovian realization, we realize non‐Markovian SDEs as a Markov process in an extended space. Unlike the established theory of Markovian realization however, the Markovian realizations here are accurate on short timescales and may be exact globally in time, when flows and fluctuations are analytic. This theory is exact for SDEs with analytic flows and fluctuations, and is approximate when flows and fluctuations are differentiable. It provides useful analysis tools, which we employ to solve linear SDEs with analytic fluctuations. It may also be useful for studying rougher SDEs, as these may be identified as the limit of smoother ones. This theory supplies effective, computationally straightforward methods for simulation, filtering and control of SDEs; among others, we rederive generalized Bayesian filtering, a state‐of‐the‐art method for time‐series analysis. Looking forward, this paper suggests that generalized coordinates have far‐reaching applications throughout stochastic differential equations.
Background: A better understanding of the neural changes associated with paresis in stroke patients could have important implications for therapeutic approaches.Dynamic Causal Modeling (DCM) for functional magnetic resonance imaging (fMRI) is commonly used for analyzing effective connectivity patterns of brain networks due to its significant property of modeling neural states behind fMRI signals.We applied this technique to analyze the differences between motor networks (MNW) activated by continuous passive movement (CPM) of paretic and non-paretic ankles in subacute stroke patients.This study aimed to identify CPM induced connectivity characteristics of the primary sensory area (S1) and the differences in extrinsic directed connections of the MNW and to explain the hemodynamic differences of brain regions of MNW.Methods: For the network analysis, we used ten stroke patients' task fMRI data collected under CPMs of both ankles.Regions for the MNW, the primary motor cortex (M1), the premotor cortex (PM), the supplementary motor area (SMA) and the S1 were defined in a data-driven way, by independent component analysis.For the network analysis of both CPMs, we compared twelve models organized into two model-families, depending on the S1 connections and input stimulus modelling.Using DCM, we evaluated the extrinsic connectivity strengths and hemodynamic parameters of both stimulations of all patients.Results: After a statistical comparison of the extrinsic connections and their modulations of the "best model", we concluded that three contralateral self-inhibitions (cM1, cS1, and cSMA), one contralateral inter-regional connection (cSMA→cM1), and one interhemispheric connection (cM1→iM1) were significantly different.Our research shows that hemodynamic parameters can be
This paper considers psychotic symptoms in terms of false inferences or beliefs.It is based on the notion that the brain is an organ of inference that actively constructs hypotheses to explain or predict its sensations.This perspective provides a normative (Bayes optimal) account of action and perception that emphasises probabilistic representations; in particular, the confidence or precision of beliefs about the world.We consider sensory attenuation deficits, catatonia and delusions as various expressions of the same core pathology: namely, an aberrant encoding of precision in a predictive coding hierarchy.In predictive coding, precision is thought to be encoded by the postsynaptic gain of neurons reporting prediction error.This suggests that both pervasive trait abnormalities and florid failures of inference in the psychotic state can be linked to factors controlling postsynaptic gain-such as NMDA receptor function and (dopaminergic) neuromodulation.We illustrate these points using a biologically plausible simulation of attribution of agency-showing how a reduction in the precision of prior beliefs, relative to sensory evidence, can lead to false inference.