James A Bisby’s research while affiliated with University College London and other places

Aberrations to metacognition—the ability to reflect on and evaluate self-performance—are a feature of poor mental health. Theoretical models of post-traumatic stress disorder propose that following severe stress or trauma, maladaptive metacognitive evaluations and appraisals of the event drive the development of symptoms. Empirical research is required in order to reveal whether disruptions to metacognition cause or contribute to symptom development in line with theoretical accounts, or are simply a consequence of ongoing psychopathology. In two experiments, using hierarchical Bayesian modelling of metacognition measured in a memory recognition task, we assessed whether distortions to metacognition occur at a state-level after an acute stress induction, and/or at a trait-level in a sample of individuals experiencing intrusive memories following traumatic stress. Results from experiment 1, an in-person laboratory-based experiment, demonstrated that heightened psychological responses to the stress induction were associated with poorer metacognitive efficiency, despite there being no overall change in metacognitive efficiency from pre- to post-stress (N = 27). Conversely, in experiment 2, an online experiment using the same metamemory task, we did not find evidence of metacognitive alterations in a transdiagnostic sample of patients with intrusive memory symptomatology following traumatic stress (N = 36, compared to 44 matched controls). Our results indicate a relationship between state-level psychological responses to stress and metacognitive alterations. The lack of evidence for pre- to post-stress differences in metamemory illustrates the importance for future studies to reveal the direction of this relationship, and consequently the duration of stress-associated metacognitive impairments and their impact on mental health.

Slow waves of neuronal activity are a fundamental component of sleep that are proposed to have homeostatic and restorative functions. Despite this, their interaction with pathology is unclear and there is only indirect evidence of their presence during wakefulness. Using intracortical recordings from the temporal lobe of 25 patients with epilepsy, we demonstrate the existence of local wake slow waves (LoWS) with key features of sleep slow waves, including a down-state of neuronal firing. Consistent with a reduction in neuronal activity, LoWS were associated with slowed cognitive processing. However, we also found that LoWS showed signatures of a homeostatic relationship with interictal epileptiform discharges (IEDs): exhibiting progressive adaptation during the build-up of network excitability before an IED and reducing the impact of subsequent IEDs on network excitability. We therefore propose an epilepsy homeostasis hypothesis: that slow waves in epilepsy reduce aberrant activity at the price of transient cognitive impairment.

Aberrations to metacognition— the ability to reflect on and evaluate self-performance— are a feature of poor mental health. Theoretical models suggest that following a stressful event, maladaptive metacognitive evaluations and appraisals of the event drive development of post-traumatic stress symptoms. Yet it is unclear whether disruptions to metacognition causes or contributes to symptom development, or are simply a consequence of ongoing psychopathology. In two studies, using hierarchical Bayesian modelling of metacognition combined with a memory encoding task, we assessed whether distortions to metacognition occur at a state-level after an acute stress induction, or at a trait-level in a sample of individuals experiencing intrusive memories following traumatic stress. Study 1 indicated that heightened perceived stress was associated with impairments in metacognitive efficiency on a memory test after a stress induction (N = 27). Study 2 demonstrated that a transdiagnostic sample of individuals experiencing intrusive memories following a traumatic stressor (N = 39) showed no significant differences in metacognitive efficiency compared to matched controls on the same memory test (N = 45). Our results show that alterations to metacognition do not occur in patients experiencing intrusive memories following traumatic stress, but instead are associated with temporary, heighted levels of acute stress. This suggests that differential sensitivity to acute stress, rather than ongoing psychopathology, induces metacognitive impairments, which could predispose individuals to future mental health problems via downstream changes to other cognitive processes.

Emotion can affect the way in which experiences are stored in our memory. The dual representation account proposes that traumatic events may be encoded as fragmented sensory-perceptual details without a broader conceptual organisation. This can result in involuntary retrieval of perceptual information triggered by environmental cues without the associated context – a phenomenon referred to as intrusive memories. Currently, it is unknown whether individuals who experience intrusive memories have an underlying vulnerability to aberrant memory encoding, which may lead to the onset or maintenance of symptoms. In Experiment 1, we examined memory recall for neutral and negative images in a transdiagnostic sample of patients with intrusive memories ( N = 36), compared to healthy controls ( N = 44). Clinical diagnoses in the patient sample included Post-Traumatic Stress Disorder, Major Depressive Disorder, Social Anxiety Disorder, Generalised Anxiety Disorder, Panic Disorder and Other Specified Feeding or Eating Disorders. We excluded participants currently taking psychotropic medication. At encoding, participants viewed neutral, negative and mixed valence image pairs. In the test phase, participants were presented with cues and, if recognised, were asked to recall the associated image. We found a significant group effect, with patients demonstrating impaired item memory for negative images [F(1,280) = 4.435, p = 0.036], relative to healthy controls. This group difference might suggest that individuals with intrusive memories experienced greater sensitivity to negative stimuli, leading to disruptions in memory encoding. Recent work highlights attention maintenance on threat and high levels of threat-related emotional arousal in anxiety- and fear-related disorders which may be one factor driving the disruption to item memory observed in our clinical population. For Experiment 2, in a separate sample of healthy participants ( N = 18) we measured eye-tracking behaviour during the encoding phase of the same task. Healthy participants showed greater item memory [F(3, 136 = 2.893, p = 0.0377] and avoidance of fixation [F(1, 110) = 4.898, p = 0.029] on highly arousing, negative stimuli relative to neutral. This might suggest that a shift in attention away from negative stimuli prevents item memory impairments for emotional information. Our future work will identify biological factors driving attentional biases and higher emotional arousal in clinical populations.