Valentina Petrolini

Autistic individuals are commonly said – and also consider themselves – to be excessively literalist, in the sense that they tend to prefer literal interpretations of words and utterances. This literalist bias seems to be fairly specific to autism and still lacks a convincing explanation. In this paper we explore a novel hypothesis that has the potential to account for the literalist bias in autism. We argue that literalism results from an atypical functioning of the predictive system: specifically, an atypical balance between predictions and error signals in language processing may make individuals more uncertain about their own predictions. Such uncertainty is then often resolved by resorting to the safest interpretation, that is, the literal one. We start by reviewing existing explanations of other autistic traits that appeal to predictive processing. We then apply these insights to language, by showing that predictions play a key role in everyday comprehension and that a low level of confidence in one’s own predictions is likely to escalate comprehension difficulties. Finally, we take a deeper look at non-literal uses of language by discussing the case of metaphors, to illustrate how a predictive processing account offers a promising explanation of the literalist bias in autism.

Vocal bursts are non-linguistic affectively-laden sounds with a crucial function in human communication, yet their affective structure is still debated. Studies showed that ratings of valence and arousal follow a V-shaped relationship in several kinds of stimuli: high arousal ratings are more likely to go on a par with very negative or very positive valence. Across two studies, we asked participants to listen to 1,008 vocal bursts and judge both how they felt when listening to the sound (i.e. core affect condition), and how the speaker felt when producing it (i.e. perception of affective quality condition). We show that a V-shaped fit outperforms a linear model in explaining the valence-arousal relationship across conditions and studies, even after equating the number of exemplars across emotion categories. Also, although subjective experience can be significantly predicted using affective quality ratings, core affect scores are significantly lower in arousal, less extreme in valence, more variable between individuals, and less reproducible between studies. Nonetheless, stimuli rated with opposite valence between conditions range from 11% (study 1) to 17% (study 2). Lastly, we demonstrate that ambiguity in valence (i.e. high between-participants variability) explains violations of the V-shape and relates to higher arousal.

Recent trends in psychiatry involve a transition from categorical to dimensional frameworks, in which the boundary between health and pathology is understood as a difference in degree rather than as a difference in kind. A major tenet of dimensional approaches is that no qualitative distinction can be made between health and pathology. As a consequence, these approaches tend to characterize such a threshold as pragmatic or conventional in nature. However, dimensional approaches to psychopathology raise several epistemological and ontological issues. First, we review major sources of evidence usually recruited in support of the dimensional trend (focusing on clinical observation and biological data), and we show that these are connected to different conceptualizations of how dimensional traits extend across health and pathology. Second, we criticize two unquestioned assumptions that stand at the core of the dimensional trend: a) that there is continuity from health to pathology at the symptomatic level; b) that such continuity reflects an underlying continuity in the genetic liability for pathological conditions. Third, we argue against the idea of a conventional threshold by showing that such a view implies a linear relationship between the genotype and the phenotype. Fourth, drawing on epigenetics and developmental biology, we offer a characterization of mental disorders as stable and dynamic constellations of multi-level variables that differ qualitatively from ‘healthy states’. We conclude by showing that our account has several theoretical advantages over both categorical and dimensional approaches. Notably, it provides crucial insights into psychological development over time and individual differences, with major implications in terms of intervention and clinical decision-making.

Characterizations of autism include multiple references to rigid or inflexible features, but the notion of rigidity itself has received little systematic discussion. In this paper we shed some light on the notion of rigidity in autism by identifying different facets of this phenomenon as discussed in the literature, such as fixed interests, insistence on sameness, inflexible adherence to routines, black-and-white mentality, intolerance of uncertainty, ritualized patterns of verbal and non-verbal behavior, literalism, and discomfort with change. Rigidity is typically approached in a disjointed fashion (i.e., facet by facet), although there are recent attempts at providing unifying explanations. Some of these attempts assume that the rigidity facets mainly relate to executive functioning: although such an approach is intuitively persuasive, we argue that there are equally plausible alternative explanations. We conclude by calling for more research on the different facets of rigidity and on how they cluster together in the autistic population, while suggesting some ways in which intervention could benefit from a finer-grained view of rigidity.

Despite several criticisms surrounding the DSM classification in psychiatry, a significant bulk of research on mental conditions still operates according to two core assumptions: a) homogeneity, that is the idea that mental conditions are sufficiently homogeneous to justify generalization; b) additive comorbidity, that is the idea that the coexistence of multiple conditions in the same individual can be interpreted as additive. In this paper we take autism research as a case study to show that, despite a plethora of criticism, psychiatric research often continues to operate in accordance with this model. Then we argue that such a model runs into problems once facts about comorbidity are taken into account. Finally, we offer some suggestions on how to tackle the challenge raised by comorbidity and its impact on heterogeneity. To do so, we explore transdiagnostic stratification accounts and network models to show that combining these approaches can move us in the right direction.

The notions of at-risk and subthreshold conditions are increasingly discussed in psychiatry to describe mild, brief, or otherwise atypical syndromes that fail to meet the criteria for clinical relevance. However, the concept of vulnerability is still underexplored in philosophy of psychiatry. This article discusses psychiatric vulnerability to clarify some conceptual issues about the various factors contributing to vulnerability, the notions of risk and protection, and the idea that there are multiple ways of crossing the threshold to clinical relevance. My goal is to lay the groundwork for a finer-grained discussion on psychiatric vulnerability that reflects the complex nature of mental conditions and illustrates the kind of thinking needed in clinical practice.

Despite several criticisms surrounding the DSM classification in psychiatry, a significant bulk of research on mental conditions still operates according to two core assumptions: a) homogeneity, that is the idea that mental conditions are sufficiently homogeneous to justify generalization; b) additive comorbidity, that is the idea that the coexistence of multiple conditions in the same individual can be interpreted as additive. In this paper we take autism research as a case study to show that, despite a plethora of criticism, psychiatric research often continues to operate in accordance with this model. Then we argue that such a model runs into problems once facts about comorbidity are taken into account. Finally, we offer some suggestions on how to tackle the challenge raised by comorbidity and its impact on heterogeneity. To do so, we explore transdiagnostic stratification accounts and network models to show that combining these approaches can move us in the right direction.

Disorders of agency could be described as cases where people encounter difficulties in assessing their own degree of responsibility or involvement with respect to a relevant action or event. These disturbances in one’s sense of agency appear to be meaningfully connected with some mental disorders and with some symptoms in particular—i.e. auditory verbal hallucinations, thought insertion, pathological guilt. A deeper understanding of these experiences may thus contribute to better identification and possibly treatment of people affected by such disorders. In this paper I explore disorders of agency to flesh out their phenomenology in more detail as well as to introduce some theoretical distinctions between them. Specifically, I argue that we may better understand disorders of agency by characterizing them as dimensional. In §1 I explore the cases of Auditory Verbal Hallucinations (AVH) and pathological guilt and I show that they lie at opposite ends of the agency spectrum (i.e. hypoagency versus hyperagency). In §2 I focus on two intermediate cases of hypo- and hyper- agency. These are situations that, despite being very similar to pathological ones, may be successfully distinguished from them in virtue of quantitative factors (e.g. duration, frequency, intensity). I first explore the phenomenon of mind wandering as an example of hypoagency, and I then discuss the phenomenon of false confessions as an example of hyperagency. While cases of hypoagency exemplify situations where people experience their own thoughts, bodies, or actions as something beyond their control, experiences of hyperagency provide an illusory sense of control over actions or events.

Several theories propose that one of the core functions of inner speech (IS) is to support subjects in the completion of cognitively effortful tasks, especially those involving executive functions (EF). In this paper we focus on two populations who notoriously encounter difficulties in performing EF tasks, namely, people diagnosed with schizophrenia who experience auditory verbal hallucinations (Sz-AVH) and people within the Autism Spectrum Conditions (ASC). We focus on these two populations because they represent two different ways in which IS can fail to help in EF tasks, which can be illustrative for other mental conditions. First, we review the main components of EF (Section 1). Then we explain the functions that IS is taken to perform in the domain of EF (Section 2) and review the evidence concerning problems about EF in the two populations of our study: Sz-AVH (Section 3) and ASC (Section 4). After this we further detail our account about what a properly functioning IS can do for both populations and how different IS profiles may impact EF performance: in the case of Sz-AVH, the uncontrolled and intrusive character of IS negatively affects EF performance, whereas in ASC, EF is not sufficiently supported by IS, given the tendency in this population to present a diminished use of IS (Section 5). We finally briefly discuss Attention Deficit/Hyperactivity Disorder (ADHD) and Developmental Language Disorders (DLD)

According to several researchers, core affect lies at the foundation of our affective lives and may be characterized as a consciously accessible state combining arousal (activated-deactivated) and valence (pleasure-displeasure). The interaction between these two dimensions is still a matter of debate. In this paper we provide a novel hypothesis concerning their interaction, by arguing that subjective arousal levels modulate the experience of a stimulus’ affective quality. All things being equal, the higher the arousal, the more a given stimulus would be experienced as pleasant (or unpleasant). While marshaling some preliminary evidence in favor of this hypothesis, we also show how it might be relevant in reframing our conception of depressive disorders (i.e., major and bipolar depression).

Bortolotti argues that we cannot distinguish delusions from other irrational beliefs in virtue of their epistemic features alone. Although her arguments are convincing, her analysis leaves an important question unanswered: What makes delusions pathological? In this paper I set out to answer this question by arguing that the pathological character of delusions arises from an executive dysfunction in a subject’s ability to detect relevance in the environment. I further suggest that this dysfunction derives from an underlying emotional imbalance—one that leads delusional subjects to regard some contextual elements as deeply puzzling or highly significant.