Inhibitory control develops in early childhood, and atypical development may be a measurable marker of risk for the later development of psychosis. Additionally, inhibitory control may be a target for intervention.

Behavioral performance on a developmentally appropriate Go/No-Go task including a frustration manipulation completed by children ages 3–5 years (early childhood; n = 107) was examined in relation to psychotic-like experiences (PLEs; ‘tween’; ages 9–12), internalizing symptoms, and externalizing symptoms self-reported at long-term follow-up (pre-adolescence; ages 8–11). ERP N200 amplitude for a subset of these children (n = 34) with electrophysiological data during the task was examined as an index of inhibitory control.

Children with lower accuracy on No-Go trials compared to Go trials in early childhood (F(1,101) = 3.976, p = 0.049), evidenced higher PLEs at the transition to adolescence 4–9 years later, reflecting a specific deficit in inhibitory control. No association was observed with internalizing or externalizing symptoms. Decreased accuracy during the frustration manipulation predicted higher internalizing, F(2,202) = 5.618, p = 0.004, and externalizing symptoms, F(2,202) = 4.663, p = 0.010. Smaller N200 amplitudes were observed on No-Go trials for those with higher PLEs, F(1,101) = 6.075, p = 0.020; no relationship was observed for internalizing or externalizing symptoms.

Long-term follow-up demonstrates for the first time a specific deficit in inhibitory control behaviorally and electrophysiology, for individuals who later report more PLEs. Decreases in task performance under frustration induction indicated risk for internalizing and externalizing symptoms. These findings suggest that pathophysiological mechanisms for psychosis are relevant and discriminable in early childhood, and further, suggest an identifiable and potentially modifiable target for early intervention.

1. (1) To explore the literature considering explanations of the co-occurrence of OCD and PTSD symptomology.

2. (2) To consider how symptoms of two mental health conditions can maintain one another and attenuate the effectiveness of evidence-based treatment for the other mental health condition.

3. (3) Consider the use of concurrent therapeutic approaches to treat co-occurring mental health conditions.

1. (1) To illustrate a digital treatment of OCD through flexible application of the current evidence base.

2. (2) To gain an understanding of the strengths and weaknesses of delivering digital out-patient CBT for OCD.

3. (3) To consider the utility of structured case reports in routine practice when delivering digital therapy.

1. (1) To illustrate the importance of understanding the person’s OCD beliefs ‘from the inside’ including the internal logic that leads to specific behaviours.

2. (2) To understand the ways that key individuals in the lives of people with OCD can become entangled with the OCD (through the best of intentions) and to provide practical clinical guidance for CBT therapists around how to engage and work with these individuals in the lives of people with OCD.

3. (3) To explain and delineate the idea of approach-supporting behaviours, distinguishing these from safety-seeking behaviours.

4. (4) To distinguish the interpersonal component of reassurance from the neutralisation component and provide guidance on how we can help family members to replace reassurance with something that is equally or more supportive whilst not maintaining the OCD.

Diminished sensory gating (SG) is a robust finding in psychotic disorders, but studies of early psychosis (EP) are rare. It is unknown whether SG deficit leads to poor neurocognitive, social, and/or real-world functioning. This study aimed to explore the longitudinal relationships between SG and these variables.

Seventy-nine EP patients and 88 healthy controls (HCs) were recruited at baseline. Thirty-three and 20 EP patients completed 12-month and 24-month follow-up, respectively. SG was measured using the auditory dual-click (S1 & S2) paradigm and quantified as P50 ratio (S2/S1) and difference (S1-S2). Cognition, real-life functioning, and symptoms were assessed using the MATRICS Consensus Cognitive Battery, Global Functioning: Social (GFS) and Role (GFR), Multnomah Community Ability Scale (MCAS), Awareness of Social Inference Test (TASIT), and the Positive and Negative Syndrome Scale (PANSS). Analysis of variance (ANOVA), chi-square, mixed model, correlation and regression analyses were used for group comparisons and relationships among variables controlling for potential confounding variables.

In EP patients, P50 ratio (p < 0.05) and difference (p < 0.001) at 24-month showed significant differences compared with that at baseline. At baseline, P50 indices (ratio, S1-S2 difference, S1) were independently associated with GFR in HCs (all p < 0.05); in EP patients, S2 amplitude was independently associated with GFS (p = 0.037). At 12-month and 24-month, P50 indices (ratio, S1, S2) was independently associated with MCAS (all p < 0.05). S1-S2 difference was a trending predictor of future function (GFS or MCAS).

SG showed progressive reduction in EP patients. P50 indices were related to real-life functioning.

In a serial compound conditioning paradigm, a sequence of several conditioned stimuli (CS) is predictive to an unconditioned stimulus (US) (e.g., CSA->CSB->US). Animal research showed that, when the US is aversive, CSA elicits the strongest conditioned response, while CSB appears redundant. These effects of primacy and proximity have never been investigated in humans.

To study the effects of temporal proximity of imminent threat and safety in serial compound conditioning.

Twenty-two participants were presented with sequences [CSA->CSB->CSC->CSD]. In 55 trials all four CS were identical vowels (e.g, [oh]), and no US was presented. In the other 55 trials, the CSA was different (CSA+, e.g., [uh]), and the CSD was followed by an electrical shock (US) 2.5 times higher than the individual pain threshold.

No ERP component distinguished between CS- and CS+ for the first three stimuli in the sequence (i.e., CSA, CSB, CSC). The last CS (CSD) elicited a strong fronto-central CNV only when it was followed by US. Moreover, already after the CSA- (which signalized that no shock would be presented on that trial) the power of alpha oscillations over the somatosensory cortex significantly increased, particularly on the side contralateral to the hand that was electrically stimulated on US trials. The alpha increment lasted up to the onset of the US.

The data indicate two possible mechanisms of adjustment to predictable threat, one of which relies on safety signals (manifested in alpha increment), and the other is related to flight response (manifested in the CNV immediately preceding the shock).

The recognition of the conditioned-unconditioned stimulus (CS-US) association in classical conditioning is referred to as contingency awareness. The neural underpinnings of contingency awareness in human fear conditioning are poorly understood.

We aimed to explore the EEG correlates of contingency awareness.

Here, we recorded electroencephalography (EEG) from a sample of 20 participants in a semantic conditioning experiment. In the acquisition phase the participants were presented with sequences of words from two semantic categories paired with tactile stimulation followed by presentation of a neutral sound (US-) ((e.g., animals -> left hand vibration -> US-, clothes -> right hand vibration -> US-). In the test phase the association violated in 50% of trials which followed by a presentation of a loud noise (US+). The participants were only instructed to listen carefully. On the basis of self-reported contingency awareness, twenty participants were divided in aware (N=12) and unaware (N=8) group.

The aware group expressed a non-lateralized effect of alpha-beta (12-23 Hz) suppression along with a more negative CNV at central channels preceding presentation of the vibration (main effect of Group). Also, CNV was more negative in expectation of US+ comparing with expectation of US- in the aware group but not in the unaware group.

The results indicate that contingency awareness is accompanied by neural patterns reflecting expectation as can be seen in the suppression of somatosensory alpha-beta activity before expected presentation of the vibration as well as in CNV in expectation of an aversive event.

Previous research indicates that traumatized individuals with post-traumatic stress disorder (PTSD) symptoms may show alterations in interpersonal distance regulation that are not evident in traumatized individuals without PTSD symptoms. However, the underlying mechanisms of these alterations are yet to be investigated. Moreover, it is not clear whether altered interpersonal distance regulation is correlated with trauma-related psychopathology.

The current study investigated behavioral and neurophysiological markers of interpersonal distance regulation as predictors of PTSD and anxiety in traumatized firefighters.

Twenty-four active-duty firefighters (M = 30.58, SD = 3.62) completed an experimental task that measures comfortable interpersonal distance. During the task, event-related potentials were recorded to assess attentional processing as reflected in the P1 and N1 components. Trauma-related psychopathology was assessed using the Clinician-Administered PTSD Scale and the state version of the State-Trait Anxiety Inventory.

Participants who did not choose a closer distance towards friends as compared to strangers experienced greater anxiety post-trauma. On a neurophysiological level, participants who showed attentional avoidance towards strangers reported more PTSD symptoms. By contrast, participants who showed hypervigilant attention towards strangers reported greater anxiety.

The results demonstrate associations between interpersonal distance regulation and psychopathology after trauma, shedding light on the underlying processes of interpersonal distance regulation in anxiety and PTSD. Future studies should re-investigate these associations in a larger sample and explore potential implications for the prevention and treatment of trauma-related psychopathology.