2026 ECNP Congress
PS02-2025Temporal misalignment as a transdiagnostic marker of instability in anxiety-related deterioration
Background
Abrupt worsening in anxiety-related states is often preceded by subtle instability rather than steady symptom accumulation, yet current models rarely integrate physiological regulation and cognitive-functional control within a single dynamical account [1–3]. In my ongoing theoretical work, psychophysiological functioning is represented as the interaction of two coupled regulatory loops: a slower physiological loop indexing sleep-autonomic-somatic regulation, and a faster functional loop indexing cognitive control, behavioural performance, and goal-directed adaptation. The present abstract focuses on one specific component of that broader framework: temporal misalignment between loops as a potential transdiagnostic marker of instability in anxiety-related deterioration. Rather than presenting a full taxonomy of mental states, the aim here is to isolate a clinically relevant coordination problem that may help explain why individuals can appear outwardly functional while approaching decompensation.
Aims
This abstract develops a clinically oriented account of cross-timescale dysregulation and asks whether lag between physiological recovery and functional mobilization may serve as an early indicator of risk before overt collapse. The goal is to generate testable predictions relevant to anxiety-spectrum deterioration, stress-related decompensation, and multimodal early-warning monitoring. More specifically, the proposal aims to link clinically familiar phenomena, such as sustained functioning under strain or apparently sudden deterioration, to measurable coordination dynamics between physiological recovery and functional control.
Methods
A conceptual dynamical model is proposed in which physiological regulation (L1) and functional adaptation (L2) are estimated from repeated multimodal measures. L1 may be indexed by sleep continuity, autonomic balance, and somatic stability, whereas L2 may be indexed by behavioural performance, subjective coping, and cognitive efficiency. Temporal misalignment is defined as the lag between dominant changes in the two loops. In the clinically important pattern of compensatory overextension, L2 remains relatively preserved or elevated while L1 deteriorates, generating hidden instability despite apparently stable outward functioning [1,2]. This formulation is compatible with repeated-measures designs using wearable physiology, ecological momentary assessment, and digital behavioural metrics. Rather than assuming linear stress accumulation, the model predicts that instability emerges when cross-timescale lag increases and becomes amplified by fluctuations in system dynamics [3,4].
Results
The model generates four clinically relevant predictions. First, anxiety-like states should often present as compensatory regimes in which functional output is temporarily maintained despite declining physiological regulation [1,2]. Second, greater loop misalignment should distinguish stable high-demand functioning from trajectories approaching panic-like or burnout-like transition. Third, identical perturbations should have stronger effects when pre-existing misalignment is high, consistent with critical-transition accounts [3,4]. Fourth, markers of instability may become detectable before mean-level collapse, supporting the possibility of earlier detection through multimodal monitoring [3–5]. These predictions are theoretical, but they specify measurable variables and falsifiable hypotheses for future longitudinal studies.
Conclusions
Cross-timescale misalignment may provide a useful bridge between clinical phenomenology and applied neuroscience in anxiety-related conditions. By reframing deterioration as a coordination problem between physiological recovery and functional control, the present proposal offers a transdiagnostic and testable perspective on early risk detection.
References
- Beck AT, Clark DA. An information processing model of anxiety: Automatic and strategic processes. Behav Res Ther. 1997;35(1):49–58.
- Thayer JF, Lane RD. Claude Bernard and the heart-brain connection: Further elaboration of a model of neurovisceral integration. Neurosci Biobehav Rev. 2009;33(2):81–88.
- Scheffer M, Bascompte J, Brock WA, et al. Early-warning signals for critical transitions. Nature. 2009;461(7260):53–59.
- Dakos V, Carpenter SR, van Nes EH, Scheffer M. Methods for detecting early warnings of critical transitions in time series illustrated using simulated ecological data. PLoS One. 2012;7(7):e41010.
- Meuret AE, Ritz T, Wilhelm FH, Roth WT. Targeting pCO₂ in asthma: Pilot evaluation of a capnometry-assisted breathing training. Appl Psychophysiol Biofeedback. 2011;36(2):83–94.