Similarities And Differences Between Autism Spectrum Disorder And Social Anxiety Disorder
Several studies have suggested that there is a link between Autism Spectrum Disorder and Social Anxiety. However, in applied settings, there is little knowledge about how to assess both diseases co-occurring in one individual, which is leading to misdiagnoses. The similarities in atypical behaviour in Autism Spectrum Disorder (ASD) and Social Anxiety Disorder (SAD) are due to social impairment however, there are differences in the expression of the social difficulties. The following review will look at the extent to which ASD and social anxiety equal each other and more importantly how they differ in their social impairment. The comorbidity can be explained by a genetic component that is accountable for proneness to social phobias and a broader autism phenotype. Furthermore, the main brain structure connected to social impairment is the amygdala. This brain structure though shows different fMRI activity depending on the disease and social motivation. Lastly, people show a different pattern of eye movement and the following eye contact shows distinct reward activation among the diseases. Looking at the genetic component is important for an early assessment, maybe even prenatally. Inspecting the neuroscientific background and cognitive component of eye-movement is important for further investigation into medical intervention with drugs, assessment methods, the understanding of social motivation in ASD and SAD and early intervention methods.
Today, one of the most common comorbid diseases occurring with Autism Spectrum Disorder (ASD) is Social Anxiety (SAD). The two main diagnostic criteria according to the DSM-5 are repetitive behaviour and significant social impairment, which means a lack of involvement in relations with others. SAD is characterized by an arbitrary fear of being negatively judged by others which leads to avoiding social situations. The avoidance of social situations can lead the individual to establish a routine that is similar to repetitive behaviour by also avoiding new people and with those new situations. As we can see these two disorders can overlap severely in behavioural patterns. So how can we ensure to correctly diagnose individuals with either distinct disorder or both disorders as comorbid but still different diseases? By looking at which symptomology overlaps in both diseases and where we can make distinctions. Therefore the following review will look closely at the social impairment of both diseases and how they are linked through genetics, brain structures and how they differ in cognitive reactions and motivation. This is important for cases where the individual falls on the edge of having a disease or scores very high on the scale and appears to have a trait for this condition. Furthermore, it is relevant for administering correct intervention methods, early diagnostics and support in familial and educational settings. In particular, ASD has been researched a lot in the past few years but there is still a vague picture of the underlying biological components.
The Genetic Component
In general, there is a higher expectation for certain psychiatric disorders of relatives of autistic individuals. One of the earliest studies conducted for identifying genetic components of ASD by Piven et al. (1997) established that there could be a broader autism phenotype. This is referring to a set of behaviour and characteristics that are autism-like and prevalent in the individual but the person does not score high enough to be diagnosed. Piven (1999) concludes it as a “milder, but qualitatively similar behavioural characteristics in non-autistic relatives.” Piven et al. (1997) previously established that parents with autistic children are more likely to have social phobias. In line with that, they also explored that broader relatives like grandparents, aunts and uncles also show elevated rates of anxiety and depression. As well as, Kleberg et al. (2016) relatives of people with ASD show an increased chance of having another person in the family with SAD. The already mentioned research supports Kerns et al. (2014) suggestion for an underlying predisposition for social phobia, which can interact with other genes and the environment of the person and develop into different directions like ASD or SAD. To complete the Hallet et al. (2013) twin- study exploring anxiety risks in twins, found that children with a twin suffering from ASD have a heightened risk for elevated anxiety symptoms in general. The rate is even higher when the twin falls into the broader autism phenotype. A child, which is clinically unaffected by ASD but has a twin with ASD, shows elevated scores of social anxiety, generalized anxiety and panic. This suggests that there could be an underlying genetic component that elevates the risk of having anxiety. For this can be looked for in prenatal assessments, if we find out more about the exact genes contributing to social impairment. This relates to the research question because it links the genetic component for social impairment to ASD in one individual, while their twin or other immediate relatives show social anxiety symptoms or SAD.
In consideration of the genetic component, research has shown that there is a high chance for an underlying genetic predisposition for ASD and there could be one for social phobias, yet it still remains unclear if anxiety is actually part of the broader autism phenotype, which is connected to a heightened difficulty of diagnosing SAD and ASD as two distinct but comorbid diseases.
The Neurological Component
There are different brain structures that are related to both ASD and social anxiety. The emotional limbic system plays a key role, especially the amygdala. The amygdala is linked to the social impairment in both diseases but in different ways. According to Shou et al. (2017), autism-impaired children show an increased volume of the left amygdala, which is associated with feelings for pleasure and unpleasure. The major link in the study between autism and social behaviour is the presence of the arginine-vasopressin system. In a low concentration, this is associated with less social behaviour. Remarkable besides that, the left amygdala shows an overgrowth in children before the second year of life, smaller functional connectivity in this area and a smaller hypothalamus, which is linked to lower level of arginine-vasopressin, which in turn is related to decreased social behaviour. Around that age, most children are diagnosed with ASD and from that point of view, we can see that deficient functioning in social situations in children with ASD is rather connected to the left hemisphere of the amygdala.
Furthermore, there is a misconnection shown between the amygdala and the prefrontal cortex. Fishman et al. (2018) found that the most severe brain abnormality is due to a disconnection between the amygdala and the prefrontal cortex. Interestingly, several studies show either that a faulty social cognition can be linked to overconnectivity as well as underconnectivity. Thus far there is no clear statement about whether overconnectivity is rather linked to either ASD or SAD and vice versa. The study conducted by Fishman et al. (2018) also shows that age influences the further development of ASD. It is shown here children establish increased connectivity with the prefrontal cortex, which is seen as a socioemotional enhancement. This has not been found in children suffering from ASD, which might affect the social impairment. This in turn negatively affects the detection of environmental stimuli of i.e. peers and friends, which then negatively affects the interpretation of social cues. On the one hand, the differences between the results of the research studies could be pointing towards maturation effects of the brain but also since the connectivity is not established, ASD children do not receive the cue and therefore maybe not realize that there is a social environment to react to. On the other hand, children with SAD still have social skills and receive the cue for a social environment that they have to react to though, they worry too much about the evaluation of their performance.
A further investigation by Herrington et al. (2017) found that amygdala volume differences can be connected to different anxiety disorders. It is shown that the volume of the right amygdala is decreased in the combination of ASD with anxiety. These differences are not necessarily connected to a deficit in social skills but rather to effectively regulating emotions during social situations. Social skills can be present in people suffering from social anxiety, however, they might feel a constant embarrassment in those situations. Additionally, Kleinhans et al. (2010) found that difficulties in interpreting facial expression are linked to increased activation in the right amygdala. Their results hint that the level of social anxiety mediates the neural response to emotional faces in ASD. This show that a comorbid occurrence of ASD and SAD is linked to increased activation of the right amygdala.
Making the completion ASD and SAD can both be traced back to the amygdala as the main contributor. Though as shown in the studies above malfunctioning in social situations in ASD can be more connected to the left hemisphere of the amygdala (Shou et al., 2017), whereas anxiety is more connected to increased connectivity of the right sphere. However, the combination of both shows increased activation in the right amygdala.
The Motivational – Emotional Component
Both people with ASD characteristics and SAD characteristics show similar atypical behaviours when it comes to establishing eye contact. A recent study by Kleberg et al. (2017) which looked at how the eye movement towards human eyes in the presence of a distractor. On one hand, it was found that a higher overlap with autistic traits is linked to a delayed orientation towards the eye, that could be explained by higher anxiety drive avoidance. On the other hand, people with social anxiety seek out an opponent’s eyes faster but also look away faster. This is important because it is a physiological aspect and can be helpful for the differentiation in clients whether they have social anxiety or ASD.
A study by Beierot et al. (2014) found that social withdrawal can be observed in people with autistic traits and social anxiety traits, which in turns can lead to social anxiety diagnose when the client, in fact, has autism. The difference between the two impairments is that people with social anxiety show the social difficulties but still might have some social skills, whereas ASD shows social awkwardness, low empathy and being unconcerned with peoples’ feelings. Physiological signs that show the own sense of social awkwardness like sweating is rarely observed in ASD. The social impairment aspect in ASD could be connected to oblivion, whereas the feeling of embarrassment in social anxiety is the main reason for awkward social situations. Furthermore, they also found that ASD people show lower levels of social anxiety when they also have low levels of empathy, which could serve as a protective factor and make them as mentioned before oblivious to their social difficulties and prevents them from having negative feelings like embarrassment. Kleberg et al. (2017) suggested that people with social anxiety want to have social contacts whereas ASD individuals do not mind the loneliness. A general limitation of assessment is the differentiation of SAD from ASD in ASD individuals because the social difficulties are overlapping. However, Bejerot et al. (2017) identify two items on one scale where people with ASD traits score higher than people with SAD traits. In laying more focus on the two items where they score differently, a correct assessment can be further ensured. Kleberg et al. (2017) also suggest that ASD caused by less social motivation, whereas SAD is caused by avoidance. They also show that adults and older children with higher intelligence are more likely to develop SAD, which could be explained by humans getting older and becoming more aware of their own social relationships and those of others. Therefore, they increasingly notice how the social impairment of ASD interferes with their life and with that develop SAD.
In conclusion, there appears to be an underlying genetic component for social phobias and a broader autism phenotype. In first degree relatives, for instance, parents to children and twins there is an elevated rate of social anxiety symptoms when a child has ASD. Due to minor differences in the environment and genetic make-up of twins ASD can occur in only one while the other only shows autistic traits and scores high in anxiety. Additionally, we can trace the phenomenon of social impairment in individuals with ASD comorbid with social anxiety back to several brain structures, but the amygdala is the one that mainly influences social motivation and emotional regulation in social settings. The current body of research shows different outcomes in terms of atypical structure and volume differences. Therefore, ASD can be more linked to deficits in the left hemisphere of the amygdala, whereas SAD is more related to increased connectivity in the right hemisphere. The combination of both, where social anxiety mediates ASD shows an elevated activation in the right hemisphere of the amygdala. Individual differences such as motivation could be accountable for this. Besides that, ASD and social anxiety show both an unusual pattern when it comes to establishing eye contact, but socially anxious people are directing their eyes towards the eyes of an opponent, however they break the eye contact quickly due to negative feelings as feedback. On the contrary, ASD shows a delay in establishing eye contact because they simply do not receive the pleasure of connecting with another human being. This also reflects that socially anxious people strive for social interaction, whereas the social impairment in ASD people makes them not mind the loneliness. When it comes to motivation this might already be connected to a different baseline in motivation. For ethical reasons and since ASD is a childhood disorder, assessment styles rely usually on parents and as they grow older, self-assessment. Kerns et al. (2014) approach was a combination of parent-assessment, self-assessment and interviews, which is time-consuming and costly but could provide the most reliable subjective and objective assessment. Mainly it can be criticized that standardized tests for ASD and SAD are oriented on normally developing children but not on children that show symptoms of both diseases. Future research could establish a better differentiation for the assessment of SAD and ASD to prevent falsely diagnosing children with ASD. More focus on the assessment of overlapping symptomology can be beneficial for cases that are on the edge of being contracted with those diseases. Further focusing on the genetic component can be beneficial early assessment and early intervention methods.
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