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Aim: The aim of this study was to evaluate the psychometric properties of a Swedish version of the Impaired Control Scale. Impaired control (IC) over alcohol consumption is a core symptom of alcohol use disorder and a predictor of treatment outcome, but measures of IC are not well utilised in clinical practice. Methods: The study comprised 250 individuals from a randomised controlled trial conducted at an adult outpatient addiction clinic in Sweden. The statistical analyses concern dimensionality, convergent and divergent validity, reliability, measurement invariance and sensitivity to change. Results: Regarding dimensionality, a principal component analysis of the standardised residuals from a Rasch model indicated some evidence of further dimensions underlying the responses in the Failed Control (FC) and Perceived Control (PC) parts. Two parallel items (12 and 22 respectively) seemed to drive potential multidimensionality. When these items were excluded, goodness of fit to one-dimensional models was improved. Tests of convergent and divergent validity showed that failed control had the strongest associations to impaired control and alcohol use disorder while the attempted control part was not associated with the construct of impaired control or alcohol use disorder. Conclusion: The present results show that the FC part is the most valid measure of the underlying construct of IC. In addition, FC had close to a large effect in regard to sensitivity to change. This suggests that the FC part has potential utility for use as an assessment and evaluation tool of treatment effect on impaired control of drinking.

Individuals with high levels of anxiety are hypothesized to have impaired executive control functions that would otherwise enable efficient filtering of irrelevant information. Pinpointing specific deficits is difficult, however, because anxious individuals may compensate for deficient control functions by allocating greater effort. Here, we used event-related-potential indices of attentional selection (the N2pc) and suppression (the PD) to determine whether high trait anxiety is associated with a deficit in preventing the misallocation of attention to salient, but irrelevant, visual search distractors. Like their low-anxiety counterparts (n = 19), highly anxious individuals (n = 19) were able to suppress the distractor, as evidenced by the presence of a PD. Critically, however, the distractor was found to trigger an earlier N2pc in the high-anxiety group but not in the low-anxiety group. These findings indicate that, whereas individuals with low anxiety can prevent distraction in a proactive fashion, anxious individuals deal with distractors only after they have diverted attention.

BackgroundStudies have shown that people with internet gaming disorder (IGD) exhibit impaired executive control of gaming cravings; however, the neural mechanisms underlying this process remain unknown. In addition, these conclusions were based on the hypothesis that brain networks are temporally static, neglecting dynamic changes in cognitive processes.MethodsResting-state fMRI data were collected from 402 subjects [162 subjects with IGD and 240 recreational game users (RGUs)]. The community structure (recruitment and integration) of the executive control network (ECN) and the basal ganglia network (BGN), which represents the reward network, of patients with IGD and RGUs were compared. Mediation effects among the different networks were analyzed.ResultsCompared to RGUs, subjects with IGD had a lower recruitment coefficient within the right ECN. Further analysis showed that only male subjects had a lower recruitment coefficient. Mediation analysis showed that the integration coefficient of the right ECN mediated the relationship between the recruitment coefficients of both the right ECN and the BGN in RGUs.ConclusionsMale subjects with IGD had a lower recruitment coefficient than RGUs, which impairing their impulse control. The mediation results suggest that top-down executive control of the ECN is absent in subjects with IGD. Together, these findings could explain why subjects with IGD exhibit impaired executive control of gaming cravings; these results have important therapeutic implications for developing effective interventions for IGD.

Most people have experienced distressing events that they would rather forget. Although memories of such events become less intrusive with time for the majority of people, those with posttraumatic stress disorder (PTSD) are afflicted by vivid, recurrent memories of their trauma. Often triggered by reminders in the daily environment, these memories can cause severe distress and impairment. We propose that difficulties with intrusive memories in PTSD arise in part from a deficit in engaging inhibitory control to suppress episodic retrieval. We tested this hypothesis by adapting the think/no-think paradigm to investigate voluntary memory suppression of aversive scenes cued by naturalistic reminders. Retrieval suppression was compromised significantly in PTSD patients, compared with trauma-exposed control participants. Furthermore, patients with the largest deficits in suppression-induced forgetting were also those with the most severe PTSD symptoms. These results raise the possibility that prefrontal mechanisms supporting inhibitory control over memory are impaired in PTSD.

We revisit the concept of synergy based on the recently translated classical book by Nikolai Bernstein (On the construction of movements, Medgiz, Moscow 1947; Latash, Bernstein’s Construction of Movements, Routledge, Abingdon 2020b) and progress in understanding the physics and neurophysiology of biological action. Two aspects of synergies are described: organizing elements into stable groups (modes) and ensuring dynamical stability of salient performance variables. The ability of the central nervous system to attenuate synergies in preparation for a quick action—anticipatory synergy adjustments—is emphasized. Recent studies have demonstrated synergies at the level of hypothetical control variables associated with spatial referent coordinates for effectors. Overall, the concept of synergies fits naturally the hierarchical scheme of control with referent coordinates with an important role played by back-coupling loops within the central nervous system and from peripheral sensory endings. Further, we review studies showing non-trivial changes in synergies with development, aging, fatigue, practice, and a variety of neurological disorders. Two aspects of impaired synergic control—impaired stability and impaired agility—are introduced. The recent generalization of the concept of synergies for non-motor domains, including perception, is discussed. We end the review with a list of unresolved and troubling issues.

Gambling disorder (GD) involves persistent risky choices despite losses, suggesting impaired impulse control. While static paradigms reveal inhibition deficits in GD, they cannot model dynamic risk-reward escalations during real gambling. This study aims to investigate whether GD involves impaired dynamic impulse control during escalating stakes and to dissociate contributions of subjective risk evaluation and trait impulsivity to this deficit. Using a sequential gambling task with 83 male patients with GD and 62 matched healthy controls (HCs), this study investigated dynamic impulse control deficits under escalating stakes. We quantified dynamic impulse control via the reward-reaction time (RT) coupling for 'continue' choices (dynamic impulse control index [DICI]) using Bayesian modeling. Risk sensitivity and risk preference were derived from stop/continue decisions. Trait impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). Regression analyses examined the modulation of DICI by risk sensitivity and trait impulsivity. Patients with GD exhibited significantly attenuated DICI versus HCs, reflecting failure to increase deliberation with escalating stakes. Computational modeling revealed markedly reduced risk sensitivity in GD despite comparable risk preference. Critically, trait impulsivity positively modulated DICI in HCs but not in GD, indicating pathological decoupling. Risk sensitivity positively predicted DICI in both groups, though significantly weaker in GD. These findings establish a triadic impairment in GD: (1) attenuated adaptive impulse control during escalation (impaired DICI), (2) deficient subjective risk weighting (reduced sensitivity), and (3) breakdown of impulsivity-based modulation of control. This reveals a dynamic, mechanism-focused pathology beyond static trait models.

Background Progressive Supranuclear Palsy (PSP) shares cognitive and behavioral changes with Parkinson's Disease (PD) that challenge their differential diagnosis, especially in early stages. Changes in inhibitory control associated with impulse control disorders are often seen in PD, and related to dopaminergic treatment. We aimed to uncover distinct neuropsychological profiles particularly in the amount and type of errors within a standard cognitive assessment protocol. Method Participants included 29 patients with diagnosis of clinically probable PSP and 41 early‐PD patients matched by disease duration. Assessment consisted of a standard 90‐minute battery of neuropsychology widely‐validated tests. We analyzed the presence of repetitions and perseverative errors across several tests: phonological and semantic fluency, Trail‐making tests A/B, verbal memory lists (immediate and delayed recall), Go/No‐Go, and Wisconsin‐card sorting test. Results were co‐variated by an attentional score. Result PSP patients exhibited significantly poorer performance than PD in verbal fluency, attention, and processing speed (TMT‐A/B). In addition, PSP showed higher frequencies of perseverative and commission errors highlighting a specific profile with decreased flexibility and impaired inhibitory control in PSP compared to early‐PD. PD patients did not use higher doses of dopaminergic treatment than PSP. Conclusion The findings underscore the diagnostic value of specific error patterns in routine tasks used for assessing cognitive profiles in neurology. These profiles could serve as a bed‐side tool to help in the early differentiation of PSP and PD, and show valuable insights into the pathophysiological mechanisms of inhibitory control in both diseases.

Borderline personality disorder (BPD) is a severe mental disorder, comprised of heterogeneous psychological and neurobiological pathologies. Here, we propose a predictive processing (PP) account of BPD to integrate these seemingly unrelated pathologies. In particular, we argue that the experience of childhood maltreatment, which is highly prevalent in BPD, leaves a developmental legacy with two facets: first, a coarse-grained, alexithymic model of self and others – leading to a rigidity and inflexibility concerning beliefs about self and others. Second, this developmental legacy leads to a loss of confidence or precision afforded beliefs about the consequences of social behavior. This results in an over reliance on sensory evidence and social feedback, with concomitant lability, impulsivity and hypersensitivity. In terms of PP, people with BPD show a distorted belief updating in response to new information with two opposing manifestations: rapid changes in beliefs and a lack of belief updating despite disconfirmatory evidence. This account of distorted information processing has the potential to explain both the instability (of affect, self-image, and interpersonal relationships) and the rigidity (of beliefs about self and others) which is typical of BPD. At the neurobiological level, we propose that enhanced levels of dopamine are associated with the increased integration of negative social feedback, and we also discuss the hypothesis of an impaired inhibitory control of the prefrontal cortex in the processing of negative social information. Our account may provide a new understanding not only of the clinical aspects of BPD, but also a unifying theory of the corresponding neurobiological pathologies. We conclude by outlining some directions for future research on the behavioral, neurobiological, and computational underpinnings of this model, and point to some clinical implications of it.

Post-traumatic stress disorder (PTSD), anxiety, and impulsive aggression are linked to transdiagnostic neurocognitive deficits. This includes impaired inhibitory control over inappropriate responses. Prior studies showed that inhibitory control can be improved by modulating the right inferior frontal gyrus (IFG) with transcranial direct current stimulation (tDCS) in combination with inhibitory control training. However, its clinical potential remains unclear. We therefore aimed to replicate a tDCS-enhanced inhibitory control training in a clinical sample and test whether this reduces stress-related mental health symptoms. In a preregistered double-blind randomized-controlled trial, 100 active-duty military personnel and post-active veterans with PTSD, anxiety, or impulsive aggression symptoms underwent a 5-session intervention where a stop-signal response inhibition training was combined with anodal tDCS over the right IFG for 20 min at 1.25 mA. Inhibitory control was evaluated with the emotional go/no-go task and implicit association test. Stress-related symptoms were assessed by self-report at baseline, post-intervention, and after 3-months and 1-year follow-ups. Active relative to sham tDCS neither influenced performance during inhibitory control training nor on assessment tasks, and did also not significantly influence self-reported symptoms of PTSD, anxiety, impulsive aggression, or depression at post-assessment or follow-up. Our results do not support the idea that anodal tDCS over the right IFG at 1.25 mA enhances response inhibition training in a clinical sample, or that this tDCS-training combination can reduce stress-related symptoms. Applying different tDCS parameters or combining tDCS with more challenging tasks might provide better conditions to modulate cognitive functioning and stress-related symptoms.

Background Control of breathing is known to be adversely affected by cognitive impairment, often associated with sleep apnea or disordered breathing during sleep in MCI/AD. The origin of this disorder is thought to be in the dysfunction of the respiratory control centers of the brainstem or in the impaired afferent signaling from cortical regions. Continuous breathing data were collected in a multi‐center study in Los Angeles (USC), Kansas City (KUMC) and Dallas (UT‐SWMC), and used to compute respiratory rate variability (RRV) to test the hypothesis that voluntary control of breathing is impaired in MCI and mild AD patients relative to cognitively normal controls, and whether this impairment is more severe in mild AD than MCI patients. Method The collected continuous breathing data were used to compute the RRV as the standard deviation of breath‐to‐breath respiratory rate variations during metronome‐guided slow‐paced breathing (6 breaths per minute) over 5 minutes under supine resting conditions for each of 61 MCI, 32 mild AD patients and 78 age/sex‐matched cognitively normal controls. The computed RRV was used to quantify and compare the voluntary control of breathing for all participants. Result The resulting p‐values of mean‐difference t‐tests were: • Controls vs. MCI patients: 0.304 (0.145) vs. 0.393 (0.222), p = 0.0039 • Controls vs. AD patients: 0.304 (0.145) vs. 0.561 (0.258), p = 2.4E‐06 • Controls vs. MCI & AD patients: 0.304 (0.145) vs. 0.451 (0.247), p = 1.7E‐06 • MCI vs. AD patients: 0.393 (0.222) vs. 0.561 (0.258), p = 0.0014 The results are shown in Figure 1 as box‐whisker plots. The p‐values showed significant mean‐differences in all four cases, with comparisons against mild AD patients showing greater differentiation. The observed mean RRV values showed stratification of impairment: 0.393 for MCI vs 0.561 for mild AD, relative to 0.304 for controls. Conclusion Quantitative analysis of a simple measure of voluntary control of breathing during metronome‐guided slow‐paced breathing under supine resting conditions showed significant mean‐differences between 61 MCI patients, 32 mild AD patients and 78 age/sex‐matched cognitively normal controls (see Figure 1), suggesting that the RRV physio‐marker has the potential to aid in the diagnosis of MCI and mild AD.