Mindfulness and Autism Spectrum Disorder:
Neuroplasticity in Empathy and Self-Reference
Autism spectrum disorder (ASD) is a neurodevelopmental disorder (Bailey, Phillips, & Rutter, 1996) with increasing prevalence (Matson & Koslowski, 2011, Dawson & Sterling, 2008). The wide range of behavioral disabilities associated with autism include difficulties in reciprocal social interactions, emotional expression, and emotional recognition (Bauminger, 2010). These deficits in social interaction correlate with parallel deficits in empathy, which may underlie impaired social function in autism and ASD (Lombardo et. Al, 2007). Current research on behavioral therapy and treatments for those suffering from ASD include, but are not limited to, enhancement of empathy and social skills (Cappadocia & Weiss, 2011). For example, mindfulness training has been used as a therapy for those suffering from autism and ASD to reduce aggression (Singh et, al, 2011), affective problems (Spek et. Al, 2013), and executive control deficits (Bögels et. Al, 2008).
However, there is a lack of research that examines the benefit of mindfulness training on empathy in those with autism. Findings from available research suggest that mindfulness training results in neuroplastic changes in brain areas that have been associated with empathy. One view is that such changes effectively strengthen signals and increase neural network function related to empathetic processes (Teper & Inzlicht, 2013, Grant et. Al, 2013, Taylor et. Al, 2011). This paper will examine evidence related to the putative neural bases of empathy as well as apparent neural deficits that may underlie altered empathy in those with autism. It will also address current mindfulness therapies and the neural changes caused by mindfulness practices. Mindfulness training could be viable therapy at the neural level to promote neurophysiological changes leading to improved empathetic responses in those with ASD. Improved empathetic responses could, in turn, result in improved behavioral and social interactions with others.
WHAT IS EMPATHY?
Empathy allows us to understand others’ feelings and actions (Bernhardt & Singer, 2012), critical in appropriate social functioning and relationship building. Empathy is when one observes and infers from another person’s emotions, which results in a shared emotional state in the observer (Bernhardt & Singer, 2012, Schulte-Ruther et al., 2011). Fundamentally, empathy is composed of an affective component that allows for “contagion”, the ability to share someone’s emotion, and a cognitive component that entails Theory of Mind (ToM) or “mentalizing” (Schulte-Ruther et al., 2011, Bird et al., 2010). ToM is a kind of self-referential cognition necessary for the evaluation of other people’s emotions in comparison to one’s own emotions (Schulte-Ruther et al., 2011).
Empathy is considered to be the culmination of affective components as well as cognitive components (Bernhardt & Singer, 2012). The cognitive self-referencing component of empathy has been linked to activity in the medial prefrontal cortex (mPFC), superior temporal sulcus, and temporoparietal junction (Bird et al., 2010). The affective component has been shown to activate somatosensory, insular, and anterior cingulate cortices, neural networks that are also involved for emotional states experienced by the self (Bird et al., 2010). For the purpose of this analysis, the anterior insula, the cingulate cortices, and the prefrontal cortex will be addressed with regard to their function. These networks are crucial for empathetic processing and poor connectivity, hyperactivity, and hypoactivity of these areas characterize neural consequences of those with ASD, to be discussed later.
The anterior insula (AI) is implicated in the affective processing limb of empathetic processes (Uddin & Menon, 2009). It is considered to act as a physical hub between cognitive processing oriented internally and externally (Uddin & Menon, 2009), thus providing communication between limbic areas and action representation networks (Carr et al., 2003). It contains substrates for awareness of environment, others, and themselves (Uddin & Menon, 2009). Thus, the anterior insula is believed to be necessary for understanding one’s own internal emotions both through detecting one’s own emotional state and by recognizing the emotional state of others in the local environment. As a critical bridge between external and internal processing, injury to this circuit is predicted to cause impaired understanding of others’ emotions and, consequently, problems in empathizing (Carr et al., 2003).
Another critical area to empathetic processing is the cingulate cortex. Specifically, the anterior cingulate cortex has been shown to have affective and cognitive subdivisions (Bush, Luu & Posner, 2000). The ACcd is thought to act as the cognitive component that attends to executive functions. The ACcd has strong reciprocal connections with the lateral prefrontal cortex, parietal cortex, and motor areas (Bush, Luu & Posner, 2000). Meanwhile, the ACad serves as the affective component that assesses salience of emotional information and regulation of responses. It is highly interconnected with the anterior insula, amygdala, hippocampus, and hypothalamus among other structures (Bush, Luu & Posner, 2000). In fMRI studies, activation of both the anterior and posterior cingulate occurs in response to decisions made in games involving two people, while middle cingulate activation is observed in response to one’s own social emotions and decisions (Chiu et al., 2009).
The prefrontal cortex (PFC) provides executive functions in connection with other empathetic areas. The ACC and the lateral PFC are involved in effortful control in social cognition (Bush, Luu & Posner, 2000). The ventromedial PFC acts as the “mentalizing system” and is activated upon empathizing with happiness and anxiety (Morelli et al., 2009). The PFC has been shown to be crucial to ToM function as well as empathetic function in fMRI studies (Völlm et al., 2006). This research suggests that the PFC provides executive control for empathetic functions, and acts as a connection between multiple empathetic networks of the brain.
Autism Spectrum Disorder
Autism spectrum disorder (ASD) is characterized by impairments in communication and language as well as the presence of restrictive behaviors and interests. However, the primary deficit seen in those suffering from ASD is one of social interaction (Dawson & Sterling, 2008, Uddin & Menon, 2009). Impairments in social interaction include poor relationships with peers and disinterest in others (isolation or avoiding interaction), impairments seen in even high functioning ASD individuals (Dawson & Sterling, 2008, Laushey & Heflin, 2000). It has been suggested that deficits in social interaction are caused by shortcomings in empathy and ToM (Lombardo et al., 2007). For example, those with ASD have difficulty understanding the intentions, beliefs, and emotions of other people (Schulte-Ruther, 2011), which could originate from difficulties with ToM demands (source) and empathy.
Impairments in self-referential cognition could also hinder empathy in ASD because without the fundamental basis of understanding of their own emotional state, they cannot accurately understand someone else’s and consequently feel that way themselves. Those affected by autism show high rates of alexithymia (Bird et al., 2010), which is the inability to identify and describe one’s own emotions (Lombardo et. al, 2007). In addition, those affected by ASD have fewer descriptions of their own emotional and mental states, don’t show improved memory for self-related events or materials, and have atypically low rates of use of first-person pronouns (Schulte-Ruther, 2011). Empathy deficits are a result of high rates of comorbidity between alexithymia and autism (Bird et al., 2010), thus the inability to reference oneself may not be a main effect of autism but a parallel symptom of alexithymia. Symptomatically, alexithymia reveals the importance of intact ToM function for empathy to emerge. Specifically, networks that are used for empathy have shared processes, some responsible for processing one’s own emotions and some that represent others’ emotions (Bird et al., 2010).
Neural impairments in areas of the brain that are centers for empathetic activity include, but are not limited to the AI, the ACC, and prefrontal cortex. Previous research suggests that autism can be defined as a connectivity disorder within the frontal cortex and other brain systems caused by disorganized, poorly synchronized, and over-extensive connectivity (Ussin & Menon, 2009). Findings suggest that individuals with ASD have hypoactivity (less than normal activity) in the AI (Uddin & Menon, 2009). As the AI appears to coordinate numerous brain network interactions, it may be that difficulties in emotional awareness are related to this hypoactivity of the AI, and data show that the more reduced the awareness of one’s own and other’s emotions, the weaker the activity in the AI (Uddin & Menon, 2009). In contrast, hyperactivation, that is, above normal activity, of the ACC has also been shown in individuals with ASD (Dichter, Felder & Bodfish, 2009, Jiao et al., 2010). One view is that hyperactivation occurs as a compensatory mechanism to contend with impaired cognitive control processes (Dichter, Felder & Bodfish, 2009). Hyperactivation, in turn, causes measurable increases in cortical thickness in the left caudal AAC (Jiao et al, 2010) in those with ASD. Thus, difficulties in emotional awareness could be caused by significantly low levels of activity in the AI, reducing communication of emotional responses, and high levels of activity of cognitive control that hinders emotional cognition.
Multiple areas of the PFC are involved in empathetic responses. The mPFC has been shown to be a region involved in self-referential cognition and mentalizing other people’s states (Lombardo et al., 2007). Interestingly, individuals affected by autism show dysfunction within medial prefrontal cortex (mPFC) (Lombardo et al., 2007). Activation in the ventro-medial PFC has been positively correlated with empathetic abilities thought to make possible “emotional bonding” with other people (Schulte-Ruther, 2011), a process important for developing ToM. In individuals with ASD, neural activation is located dorsally instead of ventrally, and these individuals exhibited reduced contagious emotional responses (Schulte-Ruther, 2011). Taken together, these findings imply that ASD individuals have irregular connectivity of their mPFC that is related to their ability to empathize, especially in regard to the cognitive component of ToM and “mentalizing” others’ emotions.
CURRENT TREATMENT FOR ASD
To treat the behavioral consequences of these empathetic and social deficits, current treatments for those with ASD focus on promoting social interaction and reducing stress in social situations. Treatment varies from promoting communication skills (Houghton et al., 2013), cognitive behavioral therapy (Cappadocia & Weiss, 2011, Moore & Davis, 2010), and promoting social skills (Odzemir, 2010, Flynn & Healy, 2012).
Research on communication skills has worked to amend the communication deficits exhibited by those affected by ASD. The Son-Rise program was developed to improve child-initiated social communication in children affected by autism, and showed significant improvements in promoting this interaction (Houghton et al., 2013).
Findings suggest that promoting social skills is also effective in the treatment of social difficulties for those with ASD. A method of using Social Stories, a concise and visually supported short story meant to enhance understanding of social situations, has been effective by putting social interactions into a simplified learning context (Ozdemir, 2010). Social skills interventions mean to promote skills necessary for building relationships with peers and others (Flynn & Healy, 2012).
Cognitive behavioral therapy (CBT) to improve social skills has been shown to be effective in including younger participants and have long periods of treatment and most promote positive outcomes (Cappadocia & Weiss, 2011). CBT has been used to treat anxiety symptoms in children with ASD, as there are high comorbidity rates of anxiety and ASD (Moore & Davis, 2010). The goals of traditional CBR are the identification of dysfunctional beliefs to change problematic behavior by creating a new template for coping (Moore & Davis, 2010). This is a particularly extensive therapy as it involves the building of behavioral, cognitive, and emotional skills before the practice phases of treatment begin (Moore & Davis, 2010).
MINDFULNESS AS A POTENTIAL THERAPY
Despite the massive array of research on areas of empathetic deficits in those with ASD, little research has been done to directly treat the neural origins of autism. The purpose of most behavioral treatment is meant to mitigate the behavioral symptoms and effects of autism. A more effective treatment could directly improve the connectivity of empathetic networks in the brain through neuroplasticity. Mindfulness is a part of the family of mental exercises aimed at enhancing the ability to maintain a target attentional or affective state (Grant et al., 2013). Mindfulness begins with focus on a physical object and shifts from the object itself, to the meaning of the object, and eventually towards objectless concentration (Sequiera & Ahmed, 2012). Mindfulness is distinctive because it begins with concentration practice initially to strengthen attentional control, and then it moves toward “open monitoring” of all sensations, thoughts, and emotions (Farb et al., 2012).
Previous findings suggest that mindfulness has a wide array of neuroplastic and social benefits. Mindfulness has been used as treatment to promote prosocial responses (Kemeny et al., 2013) and to augment emotion regulation in mood disorders (Farb et al., 2012). Individuals who practice mindfulness exhibit increased ability to empathize, greater activation of empathetic network elements, and greater frequency of prosocial responses (Kemeny et al., 2013). Mindfulness has also been used as therapy for those with ASD, but not to improve empathetic responses. Recent research has shown that mindfulness is effective for managing aggressive behavior in those with Asperger’s syndrome (Singh et al., 2011). Mindfulness has also been used as an effective affective therapy in reducing depression and anxiety in those with ASD (Speck, Ham & Nylicek, 2012). Due to the fact that mindfulness doesn’t require external analysis, mindfulness was considered more effective in ASD patients who already have trouble with communication (Speck, Ham & Nylicek, 2012).
Neuroplastic changes resulting from mindfulness have the potential to benefit those with ASD, as mindfulness promotes executive control, providing an alternative route to control emotion (Farb et al., 2012), which may prove beneficial for already impaired cognitive function. Mindfulness training is also correlated to increased lateral PFC activity in response to emotional stimuli, as cognitive resources are redeployed to less utilized sensory pathways (Farb et al., 2012). Mindfulness has also been shown to increase grey matter volume in the insula and somatosensory cortex (Farb et al., 2012). Analogs of enhanced executive control are also seen in the ACC, as acceptance of emotional states may contribute to improved executive function (Teper & Inzlicht, 2013). In healthy participants, meditators have been shown to identify their emotions more quickly and accurately than controls (Teper & Inzlicht, 2013).
Overall, mindfulness offers an alternative route of social cognition and self reference for those with ASD. The process of mindfulness requires both present attention to sensation without needing to cognitively elaborate or draw upon memory and results in equanimity, the suspension of judging experience (Farb et al., 2012). Research shows that neural activity shifts away from midline cortices and towards lateral PFC, and right insula (Farb et al, 2007). Mindfulness training resulting in shifting PFC activity may illustrate an enhanced ability to represent awareness of the present through a non-linguistic method (Farb et al., 2007). Awareness of the present moment requires viscerosomatic cortical areas to support network of identity (Farb et al., 2007). This alternative sense of self could entail that those with ASD wouldn’t need to rely on language components and would be able to improve self-recognition of emotion through an alternative self-reference.
Research also suggests that mindfulness training enhances attentional systems in the ACC and lateral PFC (Farb et al., 2012). Frontal theta activity, which increases with meditation, is considered to originate from regions such as the ACC and PFC and increases during emotional processing and sustained attention (Rubia, 2009). Mindfulness also reduces dimensional complexity and enhances fronto-parietal band connectivity, reinforcing networks of attention as well as increasing activity in PCC, ACC, and mPFC which are all necessary for emotion regulation (Rubia, 2009). Brain regions related with ToM function are also activated when those with ASD are instructed to intentionally empathize (Schulte-Ruther, 2011), thus explicit instruction during mindfulness practice to attend to empathy may alleviate hypoactivation of ToM areas in ASD individuals (Schulte-Ruther, 2011). Mindfulness practice has been shown to result in increased brain synchronicity (Sequeira & Ahmed, 2012), which might decrease disordered neural activity of those with ASD.
IMPLICATIONS FOR FUTURE RESEARCH
Previous research suggests that mindfulness training in healthy individuals has resulted in neuroplastic changes in the same empathetic circuits that suffer connectivity and deficits in those with ASD. Considering that mindfulness training has already been used as a behavioral treatment for those with ASD, developing a treatment for those with ASD through a mindfulness practice could have potential neural and behavioral benefits.
It is necessary to consider in this review that the benefits for mindfulness training for those with ASD could potentially be moderated by age. As autism is a developmental disorder, the earlier that it can be detected, the more effective treatment can be for long term benefits (Dawson & Sterling, 2008). Mindfulness would be difficult to implement for very young children, because they simply would not have the mental capacity to meditate. However, given that previous research on treatments can start at the kindergarten age (Odzemir, 2010), mindfulness in a developmentally age-appropriate format could be implemented.
Even in healthy participants, ability to engage in mindfulness practice is predicted by pre-existing brain function (Mascaro et al., 2013). Thus, mindfulness practice may only be effective for those with higher functioning ASD. Mindfulness practice may also not be effective if the connectivity of the empathetic networks are simply too underdeveloped to receive the neuroplastic benefits of mindfulness. Research suggests that individual differences in dispositional mindfulness can predict activity in neural networks that control emotion (Mondinos et al., 2010). If the AI, cingulate cortices, or PFC have defective activity, at a certain extent of dysfunction, mindfulness may not even elevate the activity to a more functional state. However, it is important to note that research on the effects of mindfulness in children with ASD to control aggressive behavior has been shown to be effective (Singh et al., 2011).
Further research should look into the neurophysiological changes that occur when those with ASD meditate, and if these practices could moderate empathetic response in individuals with ASD. The neural improvements in connectivity in the insula, cingulate cortices, and PFC are so extensive that research should be done on the potential for this treatment with those with ASD to improve empathetic networks. If mindfulness is used with behavioral treatment, mindfulness treatment could improve neural function, and behavioral treatment could be used as practice for these improved networks in another context, strengthening connections in the empathetic networks.
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