Unique and Transdiagnostic Dimensions of Reward Functioning in Attention-Deficit/Hyperactivity Disorder and Alcohol Use Disorder Symptoms

Aims Contemporary theories of attention-deficit/hyperactivity disorder (ADHD) and alcohol use disorder (AUD) emphasize core dysfunctions in reward-related processes and behaviors as pathognomonic characteristics. However, to date, it is unclear which domains of reward functioning are unique to ADHD versus AUD symptom dimensions, and which represent underlying shared correlates. Methods The current study employed secondary data analyses from a large community sample of emerging adults (N = 602; 57.3% female) and novel transdiagnostic modeling (i.e. bi-factor confirmatory factor analyses and structural equation modeling) of ADHD, AUD and shared symptom dimensions to identify unique and common reward-related dimensions: environmental suppressors, reward probability, hedonic capacity, proportionate substance-related reinforcement and delay discounting. Results The presence of environmental suppressors was the only reward-related construct that correlated with the underlying ADHD-AUD shared dimension. The AUD symptom dimension was uniquely associated with proportionate substance-related reinforcement, whereas the ADHD symptom dimension was uniquely associated with limited reward probability. No significant associations were found for delay discounting or hedonic capacity. Conclusions These novel findings highlight specific aspects of reward-related functioning in ADHD, AUD and shared symptom dimensions. In so doing, this work meaningfully advances theoretical conceptualizations of these two commonly co-occurring presentations and suggests future directions for research on transdiagnostic correlates. Future longitudinal studies should include clinical samples with diagnoses of AUD and ADHD to further identify underlying correlates over time.

Impact of brain-derived neurotrophic factor Val66Met polymorphism and response to escitalopram or paroxetine in obsessive–compulsive disorder

Objective Obsessive–compulsive disorder (OCD) is a severe psychiatric disorder characterized by its heterogeneous nature and by different dimensions of obsessive–compulsive (OC) symptoms. Serotonin reuptake inhibitors (SRIs) are used to treat OCD, but up to 40% to 60% of patients do not show a significant improvement with these medications. In this study, we aimed to test the impact of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism on the efficacy of antidepressants in OCD overall, and in relation to the different OC dimensions. Methods In a 6-month prospective treatment study, 69 Caucasian OCD patients were treated with escitalopram for 24 weeks or with escitalopram for 12 weeks followed by paroxetine for an additional 12-week period. Patients were genotyped and assessed for treatment response. The main clinical outcomes were improvement of the Yale-Brown Obsessive–Compulsive Scale score and in different OC symptom dimension scores. Results The Val/Val group comprised 43 (62%) patients, the Val/Met and Met/Met group comprised 26 (38%) patients. Forty-two patients were classified as responders at 12 weeks and 38 at 24 weeks; no significant association was found between BDNF Val66Met and SRIs response at 12 and 24 weeks. In analyses of the different OC symptom dimensions, the Met allele was associated with a slightly reduced score in the aggressive/checking dimension at 6 months (P = .048). Conclusions Our findings do not support the usefulness of BDNF Val66Met genotyping to predict overall response to treatment with SRIs in OCD; they did however suggest a better outcome at 6 months for the aggressive/checking symptom dimension for patients carrying the Met allele.

UMA LEITURA SOBRE O TRANSTORNO DE PÂNICO À LUZ DA TEORIA FREUDIANA DA ANGÚSTIA

Panic Disorder invites us to think about the clinical and cultural implications involved in structuring this type of suffering as treated by psychiatry through the DSM. By reducing the psychology of anguish to nosology, to a technical and ideological discourse, we disregard suffering as a result of new forms of subjectivation and modalizations of the social bond that contemporaneity has produced. Psychoanalysis is interested in psychological suffering in its symptom dimension, that is, considering the malaise in civilization without resorting to the processes of human subjectivation. In view of the above, this study aims to investigate the category of Panic Disorder from the Freudian work, following its clinical and theoretical path to understand the specificity of this form of suffering and its relations with anguish.

Deconstructing Negative Symptoms in Individuals at Clinical High-Risk for Psychosis: Evidence for Volitional and Diminished Emotionality Subgroups That Predict Clinical Presentation and Functional Outcome

Negative symptoms are characteristic of schizophrenia and closely linked to numerous outcomes. A body of work has sought to identify homogenous negative symptom subgroups—a strategy that can promote mechanistic understanding and precision medicine. However, our knowledge of negative symptom subgroups among individuals at clinical high-risk (CHR) for psychosis is limited. Here, we investigated distinct negative symptom profiles in a large CHR sample (N = 244) using a cluster analysis approach. Subgroups were compared on external validators that are (1) commonly observed in the schizophrenia literature and/or (2) may be particularly relevant for CHR individuals, informing early prevention and prediction. We observed 4 distinct negative symptom subgroups, including individuals with (1) lower symptom severity, (2) deficits in emotion, (3) impairments in volition, and (4) global elevations. Analyses of external validators suggested a pattern in which individuals with global impairments and volitional deficits exhibited more clinical pathology. Furthermore, the Volition group endorsed more disorganized, anxious, and depressive symptoms and impairments in functioning compared to the Emotion group. These data suggest there are unique negative symptom profiles in CHR individuals, converging with studies in schizophrenia indicating motivational deficits may be central to this symptom dimension. Furthermore, observed differences in CHR relevant external validators may help to inform early identification and treatment efforts.

Transdiagnostic Phenotyping Reveals a Host of Metacognitive Deficits Implicated in Compulsivity

Recent work suggests that obsessive-compulsive disorder (OCD) patients have a breakdown in the relationship between explicit beliefs (i.e. confidence about states) and updates to behaviour. The precise computations underlying this disconnection are unclear because case-control and transdiagnostic studies yield conflicting results. Here, a large general population sample (N = 437) completed a predictive inference task previously studied in the context of OCD. We tested if confidence, and its relationship to action and environmental evidence, were specifically associated with self-reported OCD symptoms or common to an array of psychiatric symptoms. We then investigated if a transdiagnostic approach would reveal a stronger and more specific match between metacognitive deficits and clinical phenotypes. Consistent with prior case-control work, we found that decreases in action-confidence coupling were associated with OCD symptoms, but also 5/8 of the other clinical phenotypes tested (8/8 with no correction applied). This non-specific pattern was explained by a single transdiagnostic symptom dimension characterized by compulsivity that was linked to inflated confidence and several deficits in utilizing evidence to update confidence. These data highlight the importance of metacognitive deficits for our understanding of compulsivity and underscore how transdiagnostic methods may prove a more powerful alternative over studies examining single disorders.