Self-face recognition

Face-processing abilities have been quite extensively characterized in behavioral studies of ASD (Jemel, Mottron, & Dawson, 2006). However, most neuroimaging studies of face perception in ASD have focused on emotion recognition, using unfamiliar faces, or faces of famous individuals, as stimuli. These early studies focused on the role of the fusiform gyrus, a cortical area specialized for face-processing (Kanwisher, McDermott, & Chun, 1997), and reported reductions in activity in the fusiform in individuals with ASD (Pierce, Muller, Ambrose, Allen, & Courchesne, 2001; Schultz et al., 2000). However, subsequent studies did not replicate this finding of fusiform hypoactivity during face perception in autism (Hadjikhani et al., 2004; Hadjikhani, Joseph, Snyder, & Tager-Flusberg, 2007).

While the aforementioned studies revealed possible alterations in facial information processing in individuals with ASD and in the associated neuronal circuitry, this early literature reflects a relatively strong focus on studying emotion recognition (Dawson, Webb, Carver, Panagiotides, & McPartland, 2004), rather than recognition of facial identity per se. Furthermore, some of the early results have not been replicated in later studies. Little empirical work has been devoted to examining brain responses to the self and close familiar others in autism, making it difficult to determine exactly to what extent this form of self-representation is altered in the disorder, and whether it is related more generally to other-face processing.

The ability to recognize oneself in the mirror has only been demonstrated in humans, chimpanzees (G. G. Gallup, 1970; Povinelli & Gallup, 1997), orangutans (Lethmate & Ducker, 1973), elephants (Plotnik, de Waal, & Reiss, 2006), and the bottlenose dolphin (Reiss & Marino, 2001). Evidence of the capacity for self-face recognition is thought to be indicative of an underlying self-concept (G. G. Gallup, Jr., 1977). Around two years of age, typically developing infants begin to show behavior indicating that they recognize themselves in the mirror (Amsterdam, 1972). Children with autism exhibit a developmental delay in the acquisition of this ability, although the majority of children that have been tested do eventually show evidence of self-recognition (Dawson & McKissick, 1984; Lind & Bowler, 2009; Spiker & Ricks, 1984).

The neural mechanisms subserving self-face recognition in ASD have recently been investigated in several imaging studies. An event-related potential (ERP) study examined brain responses to self, familiar, and unfamiliar faces in children with pervasive developmental disorder (PDD; this includes ASD). They found that children with PDD did not show significant differences in the early posterior negativity (EPN) or P300 components during viewing of self, familiar, or unfamiliar faces, whereas both the EPN and P300 responses in typically developing (TD) participants were enhanced in the self-face condition in comparison to the familiar-face condition (Gunji, Inagaki, Inoue, Takeshima, & Kaga, 2009). This work provides evidence for a reduced or even absent self-reference effect (i.e., enhanced memory for information encoded with reference to oneself) in patients with ASD.

One may hypothesize that this reduced sensitivity to “self” is related to the impaired attentional processing of self-referential stimuli. To test this hypothesis, a recent study investigated the neural correlates of face and name detection in ASD. Four categories of face/name stimuli were used: own, close-other, famous, and unknown. TD participants clearly showed a significant self-reference effect: higher P300 amplitude to the presentation of own face and own name than to the close-other, famous, and unknown categories, indicating preferential processing of self-related information. In contrast, detection of both own and close-other’s face and name in the group with ASD was associated with enhanced P300, suggesting similar attention allocation for self and close-other related information. These findings suggest that the self-reference effect is absent in the participants with ASD when self is compared to close-other, indicating that attention allocation in this group is modulated by personal significance (Cygan, Tacikowski, Ostaszewski, Chojnicka, & Nowicka, 2014).

Using event-related functional magnetic resonance imaging (fMRI) to measure brain responses to images of the subjects’ own face morphed with the faces of others, it was shown that while both TD children and children with ASD activated right inferior frontal gyrus when identifying images containing a greater percentage of their own face, TD children showed activation of this system during both self- and other-face processing. The groups did not demonstrate behavioral differences on the task, as both could perform the self–other discrimination and there were no significant group differences in reaction time. As children with ASD only recruited this system while viewing images containing mostly their own face, the authors concluded that children with ASD lack the shared neural representations for self and others that TD children possess (Uddin et al., 2008).

A near-infrared spectroscopy (NIRS) study also identified the right inferior frontal gyrus as being activated in response to self-faces in a group of children with ASD and TD males. This study additionally reported that children with the most severe symptoms showed lower activity in the right inferior frontal gyrus. These findings suggest that dysfunction in the right inferior frontal gyrus region, implicated across studies of self-face recognition (Devue & Bredart, 2011), may be one of the crucial neural substrates underlying ASD symptomatology (Kita et al., 2011).

Interestingly, the region of the inferior frontal gyrus is one of the anchors of the human mirror neuron system (MNS; for reviews see Iacoboni & Dapretto, 2006; Iacoboni & Mazziotta, 2007; Rizzolatti & Craighero, 2004; Uddin et al., 2007). The human MNS contains neurons with special properties that link what we see (perception) with what we do (action) and connect us to those around us by providing a neural substrate for meaningful social interaction (Gallese, Keysers, & Rizzolatti, 2004). Mirror neurons are active when we perform an action, and when we see that action being performed (Rizzolatti & Sinigaglia, 2010). By extension, when we observe the emotional states of others, we can feel the same emotion in empathy (Carr, Iacoboni, Dubeau, Mazziotta, & Lenzi, 2003; Gazzola, Aziz-Zadeh, & Keysers, 2006; Molnar-Szakacs & Overy, 2006). Based on this unique property of mirror neurons to internally simulate actions performed by others, it has been proposed that the MNS may provide the link between physical representations of the self and others (Molnar-Szakacs & Uddin, 2012, 2013; Uddin et al., 2007). Discussions of the human MNS generally refer to a network of regions, including the inferior frontal gyrus (IFG)/premotor cortex (PMC), the insular cortex (IC), primary sensory and primary motor cortices, the inferior parietal lobule (IPL), and the superior temporal sulcus (STS) (Iacoboni & Dapretto, 2006; Rizzolatti & Craighero, 2004).

Due to intense interest and study, the MNS in humans has already been associated with a wide variety of higher-level functions in addition to action representation, including imitation and imitation learning (Buccino et al., 2004; Iacoboni et al., 1999; Koski, Iacoboni, Dubeau, Woods, & Mazziotta, 2003; Molnar-Szakacs, Iacoboni, Koski, & Mazziotta, 2005), intention understanding (Gallese & Goldman, 1998; Iacoboni et al., 2005), empathy and theory of mind (ToM; Carr et al., 2003; Leslie, Johnson-Frey, & Grafton, 2004; J. H. Williams, Whiten, Suddendorf, & Perrett, 2001), self-representation (Molnar-Szakacs & Arzy, 2009; Uddin, Kaplan, Molnar-Szakacs, Zaidel, & Iacoboni, 2005; Uddin, Molnar-Szakacs, Zaidel, & Iacoboni, 2006), and the evolution of language (Arbib, 2005; Rizzolatti & Arbib, 1998). Interestingly, these cognitive functions subserved at least in part by the MNS – including imitation (Charman et al., 1997; J. H. Williams et al., 2001), empathy and ToM (Charman et al., 1997), self-representation (Lombardo, Barnes, Wheelwright, & Baron-Cohen, 2007), and language (Baltaxe & Simmons, 1977) – are all impaired to some extent in autism. In fact, dysfunction of the MNS has been proposed as a possible cause of autism (Iacoboni & Dapretto, 2006; Oberman & Ramachandran, 2007; J. H. Williams et al., 2001).

Aside from the studies described here, we have found no reports of the brain basis of self-face recognition abilities in autism, despite the strong emphasis on face perception in the autism neuroimaging literature. One recent behavioral study investigated the implicit access to physical self-representation in children with ASD and in TD children. Participants were submitted to a visual matching-to-sample task with stimuli depicting their own or other people’s body or face parts and were required to decide which of the two vertically aligned images matched the central target stimulus. The researchers found that children with ASD were less accurate compared to TD children. Interestingly, children with ASD performed the task better when they visually matched their own, compared to others’, stimuli, showing the self-advantage effect, as well as TD children (Gessaroli, Andreini, Pellegri, & Frassinetti, 2013).

In similar neuroimaging studies, using familiar faces as stimuli, no difference in fusiform gyrus activity between children with autism and TD children was found (Pierce, Haist, Sedaghat, & Courchesne, 2004; Pierce & Redcay, 2008), suggesting that when controlling for factors such as facial familiarity and motivation (Pierce et al., 2004), attention (Hadjikhani et al., 2004), and gaze fixation (Dalton et al., 2005), the fusiform gyrus does appear to engage in individuals with ASD (Nomi & Uddin, 2015). While basic rapid face identification mechanisms appear to be functional in ASD, individuals with ASD failed to engage the subcortical brain regions involved in face detection and automatic emotional face processing, suggesting a core mechanism for impaired socio-emotional processing in ASD. Neural abnormalities in this system may contribute to early-emerging deficits in social orienting and attention, the putative precursors to abnormalities in social cognition and cortical face processing specialization (Kleinhans et al., 2011).

Agency and perspective-taking

Another physical manifestation of the self is the sense of agency, or ownership of one’s actions (Gallagher, 2000). Behavioral work suggests that individuals with autism do not show deficits in action monitoring and attribution, despite significant impairments in mentalizing (David et al., 2008). David and colleagues have also demonstrated no impairments in visuospatial perspective-taking in adults with Asperger’s syndrome (David et al., 2009). Williams and colleagues report that individuals with autism did not differ from typically developing individuals in finding it easier to monitor their own agency than to monitor the agency of the experimenter. Further, both groups showed a self-reference effect, in that they recalled their own actions better than those of the experimenter (D. Williams & Happe, 2009). These studies suggest that action monitoring and agency are relatively intact in individuals with ASD.

Most recently, Grainger and colleagues (2013) explored whether individuals with ASD experience difficulties with action monitoring. Two experimental tasks examined whether adults with ASD are able to monitor their own actions online, and whether they also show typical enactment effects in memory (enhanced memory for actions they have performed compared to actions they have observed being performed). Individuals with ASD and TD participants showed a similar pattern of performance on both tasks. When required to distinguish person-caused from computer-caused changes in phenomenology, both groups found it easier to monitor their own actions compared to those of an experimenter. Both groups also showed typical enactment effects, supporting earlier findings that action monitoring is unimpaired in ASD (Grainger, Williams, & Lind, 2013).

Intentional binding is an implicit way of measuring sense of agency. Intentional binding refers to the temporal attraction between a voluntary action and its outcome (Haggard, Clark, & Kalogeras, 2002) and is thought to result from predictive signals generated by the motor system. A recent study reports reduced intentional binding in ASD, which the authors suggest may be due to altered predictive mechanisms related to action planning and monitoring (Sperduti, Pieron, Leboyer, & Zalla, 2014). Whereas studies explicitly examining sense of agency in ASD have reported no deficits, this implicit measure of “pre-reflective” agency may reflect subtle deficits in self-monitoring in this population.

As we have discussed earlier, it has been suggested that the social symptoms of ASD could be caused in part by a dysfunctional MNS (Iacoboni & Dapretto, 2006). Furthermore, some of our functional imaging (Uddin et al., 2005) and transcranial magnetic stimulation (Uddin et al., 2006) work has shown that the right IPL, a brain area that is considered to be part of the human MNS, is involved in self-recognition and self–other discrimination tasks. If autism involves a dysfunctional MNS, and the MNS is necessary for self-awareness, then mirror neuron deficits could be one explanation for deficits in self-awareness seen in ASD (U. Frith & Happe, 1999). Because the recursive activity of a functioning MNS might enable the brain to integrate visual and motor sensations into a coherent body schema, the deficits in self-awareness often seen in ASD might be caused by the same mirror neuron dysfunction. Of note, however, other work examining the MNS in ASD has produced mixed results (Hamilton, 2013).

Root and colleagues (2014) studied CL, an autistic adolescent who is profoundly fascinated with his reflection, looking in mirrors at every opportunity. They demonstrated that CL’s abnormal gait improved significantly when using a mirror for visual feedback. They also showed that both the fascination and the happiness that CL derived from looking at a computer-generated reflection diminished when a delay was introduced between the camera input and screen output. The authors believe that immediate, real-time visual feedback allows CL to integrate motor sensations with external visual ones into a coherent body schema that he cannot internally generate, perhaps due to a dysfunctional MNS (Root, Case, Burrus, & Ramachandran, 2015), as we have also previously proposed (Molnar-Szakacs & Uddin, 2012, 2013).

The majority of current research has found an intact sense of agency in individuals with autism using explicit judgments of agency (David et al., 2008). However, a recent study has revealed reduced intentional binding using implicit measures of agency (Sperduti et al., 2014). Taken together, these findings suggest that while there appears to be an intact explicit sense of agency, the diminished intentional binding in ASD participants might be due to altered predictive mechanisms, which are likely to be involved in action planning and monitoring. This explanation is in accordance with a large body of evidence documenting motor disturbances, as well as altered motor planning and action prediction, in individuals with ASD (Cattaneo et al., 2007; Martineau, Schmitz, Assaiante, Blanc, & Barthelemy, 2004; Nazarali, Glazebrook, & Elliott, 2009; Rinehart, Bradshaw, Brereton, & Tonge, 2001). In fact, a recent more general unifying theory put forth suggests that autism can be viewed as a disorder of prediction, and that several aspects of the autism phenotype may be manifestations of an underlying impairment in prediction abilities (Sinha et al., 2014). General sensorimotor impairments in autism have been documented in the domains of proprioception (Torres et al., 2013), gross and fine motor control (Bhat, Landa, & Galloway, 2011), and high-level motor planning (Gowen & Hamilton, 2013). How these deficits can contribute to specific aspects of physical self-related processing are currently under investigation. In particular, an “enactive account” (De Jaegher, 2013) posits that idiosyncratic ways in which individuals with ASD interact with the world can contribute to difficulties with self- and other-understanding.

To summarize, studies of the physical aspects of self-representation in individuals with ASD have revealed an intact ability for explicit face recognition, physical self–other distinction, and sense of agency. Further neuroimaging studies are required to explore this aspect of the disorder, as there is a dearth of empirical work on this topic. This need is further emphasized by findings that indicate some deficits in implicit aspects of physical self-recognition tasks, as well as tasks of agency that merit further exploration.

Personality traits

Self-related cognition of the evaluative type has been linked to a set of brain regions often termed “cortical midline structures” (Northoff & Bermpohl, 2004) or the “default mode network” (Gusnard, Akbudak, Shulman, & Raichle, 2001; Raichle et al., 2001). Regions typically considered to belong to this system include the medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), IPL, and medial temporal lobes (MTL) (Greicius, Krasnow, Reiss, & Menon, 2003). While the MPFC and PCC are considered core “hubs” of the default mode network (DMN), some have suggested that the network can be fractionated into subcomponents. Recently, Salomon, Levy, and Malach (2013) have proposed that the inferior and posterior parietal aspects of the DMN can be further subdivided such that some show greater involvement in self-referential judgments than others (Salomon et al., 2013). Andrews-Hanna and colleagues found that one subsystem including the dorsal MPFC, temporo-parietal junction, lateral temporal cortex, and temporal pole, is more engaged when individuals make self-referential judgments about their present situation or mental states, whereas a different subsystem comprised of the ventromedial prefrontal cortex (VMPFC), MTL, IPL, and retrosplenial cortex is more active during episodic judgments about the personal future (Andrews-Hanna, Reidler, Sepulcre, Poulin, & Buckner, 2010).

Additionally, the VMPFC shows activation during tasks requiring viewing of adjectives describing personality traits and judging whether or not they describe the self (Kelley et al., 2002). Tasks involving self-knowledge generally activate the anterior region of the rostral medial frontal cortex, which is also an area engaged by mentalizing or ToM (Amodio & Frith, 2006). The observation that both self-related and social cognitive processes appear to overlap in this midline brain structure (Tamir & Mitchell, 2010) has lent credence to simulation theories positing that individuals may use their own minds to understand the minds of others (Gallese, 2003).

Lombardo and colleagues used a paradigm involving reflective mentalizing or physical judgments about the self and other to examine self-representation in adults with autism. They found that TD participants demonstrated greater activations in VMPFC for the self-judgments than for the other judgments. Individuals with autism, on the other hand, did not show differential responses during self and other judgments in this same region. In addition, they report reduced functional connectivity between the VMPFC and ventral premotor and somatosensory cortex in individuals with autism (Lombardo et al., 2010). Furthermore, the magnitude of neural self–other distinction in VMPFC was strongly related to the severity of early childhood social impairments in autism. Individuals whose VMPFC made the largest distinction between mentalizing about self and other were least socially impaired in early childhood, while those whose VMPFC made little to no distinction between mentalizing about self and other were the most socially impaired in early childhood. This study further points to functional abnormalities in the neural systems anchored in the MPFC that are associated with self-related evaluative processing.

In a study by Kennedy and colleagues, participants performed a task where they made true/false judgments for statements (describing either personality traits or observable external characteristics) about themselves or a close other person. Individuals with autism showed reduced activity in VMPFC across judgments involving both the self and other (Kennedy & Courchesne, 2008). In a recent study investigating self-appraisal across social and academic domains in ASD, Pfeifer and colleagues found hypoactivation of the VMPFC and insular cortex (IC) in children with the disorder. This study also found that stronger activity in the mid-cingulate cortex and IC during self-appraisals was associated with better social functioning in the ASD group (Pfeifer et al., 2013). Taken together, these studies indicate a specificity in the deficit for neurally distinguishing self from other in ASD. Studies of social processing also point to medial prefrontal hypoactivity as a distinguishing feature of ASD. In an activation likelihood estimation meta-analysis of 24 neuroimaging studies examining social processing in ASD, it was also found that a region within the MPFC is hypoactive relative to TD adults (Di Martino et al., 2009).

While these studies suggest that atypical engagement of the MPFC, and perhaps the larger DMN, is associated with altered self-related evaluative processing in ASD, growing literature supports the idea that in such a complex disorder, it is likely that atypical neural connectivity within and between large-scale brain networks, rather than focal deficits, underlie the symptoms (Belmonte et al., 2004; Kana, Libero, & Moore, 2011; Kennedy & Adolphs, 2012; Minshew & Williams, 2007; Uddin & Menon, 2009). Several studies have found that functional connectivity of the DMN is reduced in adults and adolescents with the disorder (Assaf et al., 2010; Cherkassky et al., 2006; Kennedy et al., 2006; Monk et al., 2009; Weng et al., 2010). However, contrary to what has been reported in adults and adolescents, childhood ASD may be characterized by greater instances of hyperconnectivity than hypoconnectivity (Supekar et al., 2013; Uddin et al., 2013). Most recently, Lynch and colleagues found that the PCC was hyperconnected with the medial and anterior temporal cortex in children with ASD, and this hyperconnectivity was linked with severity of social symptoms (Lynch et al., 2013). This work lends further support to the notion that atypical patterns of DMN connectivity in ASD may lead to disrupted interactions at the neural level that could underlie social deficits in the disorder (Assaf et al., 2010; Washington et al., 2014).

We have recently proposed that simulation-based mechanisms of self- and other-understanding are supported by interactions of the human MNS with the DMN (Molnar-Szakacs & Uddin, 2012, 2013). These interactions produce the appropriate mappings to provide a coherent self-representation in the service of social-cognitive demands. Although the precise functional properties of the DMN are not yet established, a growing number of studies implicate this network in various aspects of self-related processing. For example, the DMN is implicated during self-related evaluations (Buckner & Carroll, 2007; Northoff et al., 2006) and episodic and autobiographical memories (Sestieri, Corbetta, Romani, & Shulman, 2011; Spreng, Mar, & Kim, 2009).

Simulation-based representations serve to scaffold conceptual representations that allow us to understand the self in its social context. By virtue of their differential patterns of connectivity, subdivisions of the DMN can interact with the MNS. We proposed that two of the most important hubs for interaction between the DMN and MNS are the IC and the PCC, given their unique positions as “hubs” critical for information flow throughout the entire brain (Honey, Kotter, Breakspear, & Sporns, 2007; Menon & Uddin, 2010; Molnar-Szakacs & Uddin, 2013).

A recent meta-analysis of 87 self-related studies has lent further support to the view that high-level social cognitive processes such as mentalizing engage both the MPFC and circuitry involved in low-level embodied sensorimotor representations (Qin & Northoff, 2011). The role of somatosensory cortex in low-level shared representations of touch (Blakemore, Bristow, Bird, Frith, & Ward, 2005; Keysers et al., 2004), self-experienced pain (Singer et al., 2004), and action–perception mirroring (Gazzola et al., 2006) is well established. Thus, the observation that the primary somatosensory cortex is also recruited for mentalizing about self and others suggests that low-level embodied simulative representations computed by this region are also important for the processes underlying higher-level inference-based mentalizing when compared with reflecting on physical characteristics (Lombardo et al., 2010). Taken together, these results provide strong evidence of the integration of function between the DMN and the MNS and suggest that disruptions to these inter-network interactions may underlie some of the self-related processing abnormalities in ASD (Uddin & Menon, 2009; Uddin et al., 2014).

Alexithymia, or reduced ability to identify and describe one’s emotions, often co-occurs with autism. Using functional neuroimaging, Silani and colleagues showed that high levels of alexithymia were associated with hypoactivation in the anterior insula in individuals with high-functioning autism (Silani et al., 2008). Furthermore, there was a significant correlation between activity in the insular cortex not only with alexithymia scores, but also with scores on empathic concern and perspective-taking scales. In a more recent study, the same authors measured empathic brain responses in participants with ASD and neurotypical controls while they witnessed another person experiencing pain. The results were consistent with those of the original study, showing that the levels of alexithymia, but not a diagnosis of autism, were associated with the degree of empathic brain activation in anterior insula (Bird et al., 2010). These results are important in showing that the empathy deficit widely attributed to ASD can be explained by the extent of alexithymic traits and does not necessarily constitute a universal social impairment in autism (Molnar-Szakacs & Heaton, 2012). These examples further highlight the ways in which self-representations (e.g., representations of one’s own emotions) can relate to other-representations (e.g., empathy for another’s pain) in ASD, and help us to better understand the precise nature of deficits in ASD.

Autobiographical memory and the temporally extended self

A critical aspect of self-related cognition is the ability to remember events from one’s past. It has been suggested that individuals with autism experience difficulties with accessing specific autobiographical memories due to problems in using the self as an effective memory organizational system (Crane, Goddard, & Pring, 2009). In a study examining narratives of self-defining and everyday autobiographical memories in adults with ASD, it was shown that individuals with ASD generated fewer specific memories than TD controls. Individuals with ASD also extracted less meaning from their memories than controls, which the authors interpreted as a failure in using past experiences to update the self (Crane, Goddard, & Pring, 2010).

Bruck and colleagues report that children with ASD also have autobiographical memory recall that is marked by errors of omission, and that memory is particularly poor for early life events (Bruck, London, Landa, & Goodman, 2007). A recent case report examined the development of autobiographical memory in an 8-year-old boy with Asperger’s syndrome. This child exhibited difficulties in strategic retrieval and ToM, as well as different patterns of performance with regards to autobiographical memory measured at three time points. The child showed (1) relative preservation of current year personal knowledge, but impairment for the previous and earlier years, and (2) impairment of episodic memory for the current and previous year, but performances similar to those of controls for the earlier years. The authors suggest that the abnormal functioning of social cognition in ASD, encompassing social, and personal points of view, has an impact on autobiographical memory (Bon et al., 2012).

The most recent study on autobiographical memory in children with ASD has found that a deficit in specific memory retrieval in the ASD group was more characteristic of male participants. Females in both the TD and ASD groups generated more detailed and emotional memories than males. There was also evidence of enhanced recall of recent events in females with ASD as their recent memories were more detailed than their remote memories. Girls also demonstrated superior verbal fluency scores (Goddard et al., 2014). Further research is required to study the developmental implications of these results on social behavior in children with ASD.

In neurotypical adults, autobiographical memory retrieval is associated with activation in the retrosplenial cortex and MPFC (Schacter & Addis, 2007), areas that are part of the DMN (Raichle et al., 2001). A growing number of studies suggest the brain’s default network becomes engaged when individuals recall their personal past or simulate their future (Buckner & Carroll, 2007; Molnar-Szakacs & Arzy, 2009). Recent reports of heterogeneity within the network raise the possibility that these autobiographical processes are comprised of multiple component processes, each supported by distinct functional–anatomic subsystems. Andrews-Hanna and colleagues hypothesized that a medial temporal subsystem contributes to autobiographical memory and future thought by enabling individuals to retrieve prior information and bind this information into a mental scene, and conversely, a dorsal medial subsystem was proposed to support social-reflective aspects of autobiographical thought, allowing individuals to reflect on the mental states of one’s self and others (i.e., “mentalizing”). They report that, across studies, laboratory-based episodic retrieval tasks were preferentially linked to the medial temporal subsystem, while mentalizing tasks were preferentially linked to the dorsal medial subsystem. In turn, autobiographical tasks engaged aspects of both subsystems. These results suggest the DMN is a heterogeneous brain system whose subsystems support distinct component processes of autobiographical thought (Andrews-Hanna, Saxe, & Yarkoni, 2014). Despite considerable evidence for impaired autobiographical memory in autism, no imaging studies of autobiographical memory in individuals with the disorder have yet been reported.

A recent set of reviews argue that individuals with ASD have reduced psychological self-knowledge resulting in a less elaborate self-concept. This is thought to contribute to impairments in autobiographical memory and a reduced self-reference effect. These deficits are thought to result in a diminished temporally extended self-concept in autism (Lind, 2010), specifically due to narrative memory deficits (Brezis, 2015).