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OBJECTIVE: We examined how youth self-efficacy, motivation for treatment, social support, and therapeutic alliance relate to psychotherapy outcomes of patients receiving services at outpatient community clinics. We hypothesized that (1) these variables would increase throughout the course of therapy, (2) baseline scores would predict initial ratings of distress, (3) baseline scores would predict the rate of change in symptoms throughout treatment, and (4) changes in these variables would be associated with symptom change over the course of treatment. METHOD: Participants included 150 adolescents at community outpatient treatment centers. Data was collected prior to beginning treatment, and every three weeks afterward until termination. We used hierarchical linear modeling (HLM) to address our hypotheses. RESULTS: We found that (1) youth ratings of self-efficacy, social support, and motivation increased throughout treatment, (2) initial self-efficacy and social support were associated with initial levels of distress, (3) ratings of youth self-efficacy at intake predicted its rate of change over therapy, and (4) changes in all variables during therapy were related to lower distress at termination. DISCUSSION: Results suggest that these variables may affect the trajectory and course of treatment in community-based treatment settings. These results may have implications for treatment planning to maximize treatment effectiveness.
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Several models of anxiety in autistic adults have focused on the role of intolerance of uncertainty which has biological and evolutionary bases, as a cognitive explanation for the high prevalence of anxiety in autism. This framework suggests that all people are born with a healthy level of intolerance of uncertainty, and as we develop, this intolerance is lessened as we learn when situations are safe and begin to understand and manage the uncertainty. This process of learning about managing uncertainty does not happen in the same way in those who are high in autistic traits, which could be the reason for the high levels of anxiety symptoms commonly seen in this population. We examined archival data of 199 non-autistic and 55 autistic adults from prior studies in which we collected self-report measures of autistic traits, intolerance of uncertainty, sensory processing, and anxiety. We conducted two path analyses to examine the role of intolerance of uncertainty in anxiety in autistic adults. The first model tested the idea that intolerance of uncertainty, an evolutionary phenomenon common for all people, could explain some of the cognitive aspects of anxiety in autism. The second model suggests that primary neurodevelopmental differences associated with autistic traits underlie the sensory sensitivity and sensory seeking behaviors, which in turn increase intolerance of uncertainty and subsequent anxiety. We found that the "neurodevelopmental" model had better model fit than the "evolutionary stress" model, suggesting that the neurodevelopmental impact of higher levels of autistic traits could moderate a non-autistic trajectory of learning to manage uncertainty as children develop and understand that uncertainty is common and acceptable.
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BACKGROUND: Anxiety is the most common comorbid psychiatric concern in individuals diagnosed with autism spectrum disorder (ASD) and can cause significant functional impairment. Fear conditioning tasks offer a useful neurodevelopmental model for anxiety, yet there are no published neuroimaging studies of fear conditioning using ASD samples. METHODS: Twenty adults diagnosed with ASD and 19 healthy adult control subjects completed a standard fear conditioning and extinction paradigm while undergoing functional magnetic resonance imaging scanning. A burst of air on the base of the neck was the unconditioned stimulus. Participants returned 1 day later for scanning during an extinction recall phase. A priori regions of interest were analyzed with a familywise error correction rate < 0.05. RESULTS: All regions of interest demonstrated significantly greater response to threat than safe conditions during initial fear acquisition. Compared with age-matched control subjects, the ASD group showed a significantly decreased differential response to threat versus safe cues in right amygdala during the initial fear acquisition phase and decreased response in left amygdala during the first run of extinction recall on the second day of scanning. CONCLUSIONS: Symptoms of severe anxiety in ASD may arise from atypical neural mechanisms especially related to the differentiation of threat versus safe cues. An inability to effectively identify safety contexts may underlie chronically increased levels of anxiety in many individuals diagnosed with ASD.
