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The theory of mind (ToM) has been instrumental in shaping research in psychology, neuroscience, and artificial intelligence, providing a theoretical framework for investigating the cognitive processes underlying social interaction and communication.
Social cognitive deficits appear to be a core cognitive phenotype of many clinical conditions (Cotter et al. 2018). Early work in social cognition focused on the central role of ToM impairments as a hallmark feature of ASD (Baron-Cohen, Leslie, Frith 1985; Happe & Frith 1996). Subsequently, ToM impairments have been reported in over 30 different disorders: ASD, ADHD, intellectual disability, specific language impairment (children); psychosis, schizophrenia, bipolar disorder, major depressive disorder, borderline personality disorder, generalised anxiety disorder, obsessive-compulsive disorder, panic disorder, social phobia, post-traumatic stress disorder, anorexia nervosa, bulimia nervosa, alcohol use disorder, substance use disorder (non-alcohol); multiple sclerosis, Alzheimer’s disease, amyotrophic lateral sclerosis, behavioural variant frontotemporal dementia, frontal lobe epilepsy, idiopathic generalised epilepsy, temporal lobe epilepsy, Huntington’s disease, mild cognitive impairment, Parkinson’s disease, traumatic brain injury (Cotter et al. 2018); and Tourette syndrome (Pérez-Vigil et al. 2024).
Within specific conditions, the severity of deficits in facial emotion recognition and ToM task performance appears broadly comparable, suggesting that patients with certain disorders face similar levels of difficulty across these social cognitive domains. Among individuals with neurological or developmental disorders, deficits across both task types are in the medium-to-large range. Individuals with psychiatric disorders exhibit wider variation in the severity of these deficits, potentially due to greater variability in disease state and severity. The greatest impairments are observed in patients with neurodegenerative disorders, though large deficits are also present in people with psychotic disorders (Cotter et al. 2018).
ToM in ASD and ADHD
ToM deficits are a shared feature of ASD and ADHD but differ in their underlying mechanisms and manifestations. ADHD is characterised by consistent ToM impairments across age and gender (Nejati 2022). In ASD, ToM difficulties are intrinsically linked to autism core symptoms (Lukito 2017). Co-occurring ASD and ADHD amplify challenges in ToM, metacognition, and emotional/behavioural regulation (Rosello et al. 2023; Berenguer et al. 2018).
ToM in Developmental Language Disorder (DLD)
Children with ASD have a fundamental difficulty in ToM that is independent of their language abilities. Children with DLD exhibit difficulties in everyday social interactions that involve ToM. Both ASD and language disorders may influence ToM development, suggesting that different developmental routes affect the acquisition of ToM (Schwartz, Offek, Segal 2022).
ToM in Psychosis
Psychotic experiences (PE) are associated with poorer ToM and an external locus of control,[1] as well as proportionally more self-reported ASD traits in young adulthood (Carey et al. 2021). Clemmensen et al. (2014) analysed data from two large general population samples of Danish and Dutch children and found that, cross-sectionally, PE was associated with lower scores on a ToM task in Danish children and higher scores on a ToM task in both Danish and Dutch children (hyperToM),[2] particularly when paranoid delusions were reported.
ToM in Schizophrenia
Research consistently identifies significant and persistent ToM deficits as core cognitive impairments in schizophrenia, contributing to impaired social functioning (Savla et al. 2013; Kohler et al. 2010). These deficits, including challenges in emotion recognition and reasoning about others’ mental states, remain evident even during remission phases, suggesting they are trait markers of the disorder (Sprong et al. 2007; Bora et al. 2009). While intellectual impairments partially explain ToM difficulties during remission, mentalising deficits persist independently of general cognition (Bora et al. 2009).
Comparisons Between Schizophrenia and ASD
Both schizophrenia and ASD exhibit ToM deficits, though their underlying mechanisms differ. Chung et al. (2014) conducted a meta-analysis revealing that adults with both conditions show similarly large impairments in verbal and visual mentalising tasks. However, adults with schizophrenia have greater difficulties with verbal tasks, while impairments in ASD are consistent across task types. Mazza et al. (2022) further distinguished these groups by advanced ToM tasks, where schizophrenia patients struggled to understand social scenarios, while ASD individuals misinterpreted protagonists’ intentions. This distinction highlights the nuanced differences in mentalising impairments between the two disorders.[3]
ToM in Borderline Personality Disorder (BPD)
Individuals with BPD exhibit ToM impairments primarily characterised by mistrust and negativity bias. Lévay et al. (2021) found that, compared to healthy controls, individuals with BPD expected significantly more selfishness and malevolence from others. This negativity bias may stem from early adverse environments, such as abusive family dynamics, where cooperative behaviour was often met with selfishness.
ToM impairments in BPD differ from those in ASD. While individuals with ASD struggle with intuitive mental state attribution, BPD is marked by an altered perception of others’ intentions, often assuming malevolence. Vegni, D’Ardia, Torregiani (2021) argue that while both BPD and ASD share deficits in empathy and mentalising, BPD is uniquely characterised by difficulties in distinguishing representation from reality and in integrating emotional and mental experiences into coherent self-narratives. These deficits may be linked to adverse developmental environments and underlying metacognitive dysfunctions.
ToM in Multiple Sclerosis (MS)
Cognitive dysfunction is present in up to 70% of patients with multiple sclerosis (MS) and has been reported at all stages and in all subtypes of the disease (Langdon 2011; Prakash et al. 2008; Ruet et al. 2013). Deficits are most commonly reported in attention, processing speed, memory, and executive function (Chiaravalloti & DeLuca 2008).
Individuals with MS show significant deficits in ToM and facial emotion recognition compared to healthy controls. These deficits are especially pronounced in visual ToM tasks and recognising negative emotions such as sadness, fear, and anger. They affect interpersonal skills like empathy and are linked to reduced social and psychological quality of life. Social cognitive impairments are often observed early in the disease and are comparable in magnitude to other cognitive deficits in MS, such as memory and attention issues.
Social cognitive deficits may be associated with neurocognitive dysfunction and MS-specific neurological damage. No significant relationship has been found between global cognitive impairment and ToM performance, suggesting unique contributions of MS-related brain changes. Current studies focus mainly on relapsing-remitting MS, with limited data on progressive MS or severe physical disability (Cotter et al. 2016).
ToM in Neurodegenerative Disorders
Individuals with different neurodegenerative diseases present distinct patterns of ToM deficits based on how different neuropathological processes affect the neural bases of ToM components during disease progression. There is evidence of deficits in the cognitive ToM component in cortical (e.g., Alzheimer’s disease and frontotemporal dementia) and frontal-subcortical (e.g., amyotrophic lateral sclerosis and basal ganglia disorders) neurodegenerative diseases. The affective ToM component appears markedly impaired in frontotemporal dementia. Performances on tasks assessing affective ToM are heterogeneous in Parkinson’s disease and amyotrophic lateral sclerosis (Poletti, Enrici, Adenzato 2012).
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Dysfunctional ToM has been proposed as a transdiagnostic clinical marker (Cotter et al., 2018) and has been included as a subconstruct in the Research Domain Criteria, a research framework for investigating mental disorders (Cuthbert 2014). The underlying mechanisms and the precise role of ToM in the etiology, diagnosis and treatment of these mental disorders remain poorly understood (Sprung et al. 2022).
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[1] Locus of control is a psychological concept that describes a person's belief about the causes of events in their life.
[2] Hyper Theory of Mind (HyperToM) refers to an exaggerated or excessive tendency to attribute mental states to others, meaning someone over-interprets and over-infers the thoughts and feelings of people around them, that often leads to inaccurate conclusions about their mental states; this concept is primarily studied in relation to potential risk factors for psychosis and delusional thinking.
[3] Given the overlapping yet distinct ToM deficits in schizophrenia and ASD, differential diagnosis is essential. Understanding unique patterns of ToM, such as verbal vs. visual mentalising impairments and advanced ToM task performance, can refine screening and intervention strategies (Mazza et al., 2022).
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