Measuring the cognitive abilities of autistic people and people with SSDs is a potential tool for explaining relationships between genetics, brain and phenotype (Cannon, van Erp & Glahn 2002).
One area of cognitive overlap between autism, SSD and related dimensional traits is lower executive functioning (Green, Boyle & Raine 2008; Happe, Booth, Charlton & Hughes 2006; Hill 2004; Ozonoff & Jensen 1999)“ which is understood as the set of abilities required to effortfully guide behavior toward a goal, especially in nonroutine situations (Banich 2009). In psychiatric disorders, executive functioning impairments are a major predictor of real-life functional outcomes and degree of disability (Royall et al. 2002). Poor executive functioning in schizophrenia and SPD is linked to negative symptoms, social impairment and odd speech (Diforio, Walker & Kestler 2000). Poor executive functioning in these conditions is evident on the Wisconsin card sorting test, where poor performance in autism and SSD is particularly linked to perseverationpersisting in the same behavior instead of adapting to new goals and circumstances in the test. (Goldstein, Minshew, Allen & Seaton 2002; Raine et al. 1992; Sanders et al. 2008; Tallent and Gooding 1999).
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Another well-studied area of cognitive overlap between ASC and SSD is significantly impaired working memorythe ability to retain and work with information in the short termand especially visual spatial working memory (Rosell et al. 2014; Sanders et al 2008; Schuh & Eigsti 2012). In one study, working memory accounted for other cognitive deficits in SPD, which according to the authors suggests it may be a core schizophrenia spectrum impairment (Mitropolou et al. 2015). In autism, impaired working memory is related to significant variance in language skills and prominence of autistic symptoms (Schuh & Eigsti 2012).
A promising, but relatively overlooked area of overlap in cognition is the slower processing speed associated with both autism and SSD. Both autism (Eack et al. 2013; Goldstein et al 2002; Karalunas et al. 2018; Nader, Jelenic & Soulieres 2015) and SSD (Dickinson, Ramsey & Gold 2007; Eack et al. 2013; Goldstein et al 2002; Matsui, Sumiyoshi, Kato, Yoneyama & Kurachi 2004; Mollon, David, Zammit, Lewis & Reichenberg 2018) are related to major reduction in processing speed. However, handwriting is often an integral part of processing speed tests (Benedict et al 2017) and autism is associated with impaired motor abilities (Duffield et al. 2013) and sometimes dysgraphia (poor handwriting), which is a potential confound.
However, conclusions about cognition in ASC and SSD should be mindful of individual cognitive variation between these groups, which can be considerable. Goldstein et al. (2002) found that while on a group level autism may appear cognitively similar to schizophrenia, they only resemble a minority of schizophrenic individuals. This similarity was driven by a schizophrenic subgroup which exhibited a mix of impaired and unimpaired abilities, lower verbal comprehension and elevation on the block design subtest, a profile typical of autism.
Autism and schizophrenia spectrum conditions not only have similarities (and differences) in the structure and function of the brain, but these are also related to common characteristics between the conditions.
There are both significant similarities and differences between ASC and SSD in the volume of gray matter or general size of certain structures of the brain. First, there are major differences between the two in the volume of gray matter in the frontal lobes over time. Schizophrenia is associated with deterioration of the frontal lobes (Siever & Davis 2004). By contrast, the cortex in autism can be either thicker or thinner than in typically developing people depending on when brain imaging is done during their life span (Zielinski et al. 2014). However, both spectra have less gray matter in the limbic-striato-thalamic circuitry than do controls (Cheung et al. 2010). However, psychosis in those with autism may show present a different neuroanatomical pathway. A small MRI study found that those with both autism and psychosis have reduced gray matter in several regions which was not found in those with autism or psychosis alone (Toal et al. 2009).
There are also multiple regions of the brain where ASC and SSD have similarities in white matter microstructure, though few studies compare them directly.
Studying the white matter of the corpus callosum may be promising for understanding social behavior of some individuals with autism or SSD. Schizophrenia is linked with reduced fractional anisotropy (a measure of the integrity of white matter structure) in the corpus callosum (Melicher et al. 2015; Volpe et al. 2008) which is also found in autistic individuals (Shukla, Keehn & M??ller 2010). This may be specific to a subgroup of autistic individuals that had reduced white matter integrity in the corpus callosum and reduced processing speed (Alexander et al. 2007).
Decreased fractional anisotropy of the inferior longitudinal fasciculusa white matter tractis also found in autism (Koldewyn 2014; Shukla et al. 2011) and various schizophrenia-related groups (Karlsgodt 2009; Melicher et al. 2015; Sun et al. 2016) In those at ultra-high risk for developing psychosis (Karlsgodt 2009) lower FA is linked to deterioration in social relationships at follow-up, and in schizotypal personality disorder it is linked to self-reported social isolation and avoidance (Sun et al. 2016). This suggests investigation of the role of the inferior longitudinal fasciculus in social functioning for ASC and SSD is warranted.
Genetic studies of ASC and SSD also reveal interesting relationships. Genetic relationships between schizophrenia & autism are typically associated with copy number variantsvarying numbers of repeated base pair sequences in the DNA of a gene (Guilmatre et al. 2009) more often than specific alleles. It is also not uncommon for a duplication in one gene to be linked to ASC while a deletion in the same is linked to SSD or vice-versa, implying that some mechanisms behind SSD and ASC or opposites to each other (Chisholm et al. 2015).
Both ASC and SSD also share genetic links in regions associated with certain neuroanatomical structures or features. Multiple genes related to synapses have copy number variants linked to autism, schizophrenia and intellectual disability (which is occurs at an elevated rate in autism) (Guilmatre et al. 2009). Another finding is that some individuals with autism or schizophrenia, mutations in genes for oxytocin and oxytocin receptors have been found. Oxytocin is very important for social interaction, and administration has also improved positive and negative symptoms in schizophrenia (Cochran et al. 2013).
There are also possible differences in brain function between autism and SSD, which is particularly evident in social cognition tasks. During tests of facial emotion recognition both autism and schizophrenia show reduced activation of the medial prefrontal cortex (Sugranyes, Kyriakopoulos, Corrigall, Taylor & Frangou 2011) and during a social judgement task those with SPD showed greater activation in the amygdala and clusters of the brain located in the cerebellum and intraparietal sulcus (Stanfield et al. 2017).
Finally, both spectra share many of the same correlations with prenatal and early post-natal environmental factors, such as gestational diabetes (Chisholm et al. 2015).
While there has been a lot of progress on understanding the relationship between autism spectrum conditions and schizophrenia spectrum disorders, there are still many ways our current understanding can be improved and an unmet need for clinical applications of the research.
One issue is that there are many interfering variables associated with studies of schizophrenia, yet schizophrenia is compared to autism far more frequently than with other schizophrenia spectrum samples. People with schizophrenia often undergo long term and or recurring hospitalization, take antipsychotics and suffer ongoing stress from psychosis (Dickey, McCarley & Shenton 2002). Not only can this affect behavior but the brain itself; for example antipsychotics may contribute to enlargement of the ventricles and loss of gray matter (Fusar-Poli et al. 2013). Schizophrenia is also characterized by ongoing deterioration of the brain after onset, so it may be difficult to differentiate which neuroanatomical factors existed prior to the full onset of psychosis (Pantelis et al. 2003; Pantelis et al. 2010). To avoid these issues a useful comparison group to autism may be schizotypal personality disorder. Schizotypal personality disorder is a condition with strong genetic and and neurological similarities to schizophrenia (Dickey et al. 2002) along with attenuated schizophrenia-like symptoms such as milder perceptual abnormalities, paranoia and unusual ideas (ex. that one influences events with their thoughts. Unlike in schizophrenia, psychosis is absent (aside from occasional transient symptoms) and most individuals do not use antipsychotics.
In some ways, SPD may also be more comparable with autism than schizophrenia. Individuals with SPD generally have relatively stable symptoms after onset (though with a somewhat elevated risk of schizophrenia psychosis) and criteria include interpersonal problems. In fact, though by current DSM 5 criteria autism cannot be diagnosed with SPD, autism may be more common in those with SPD (Chen 2017; Rosell et al. 2014) so investigating overlap SPD may have direct relevance to those on the autism spectrum.
Those with SPD also have neuroanatomical difference from both those with schizophrenia and typically developing controls which merit comparison with autism. It is thought these neuroanatomical difference may protect against psychosis (Downhill et al 2014; Hazlett et al. 2012, Rosell et al. 2014), so a potential future study could identify if any of these features are also present in autism and, if so, whether they might reduce impairment.
Perhaps more importantly, individual variation within those with ASC and SSD may compromise the generalizability of the research. Chisholm et al. (2015) states that research is consistent with 2 schizophrenia subgroups, one that was relatively normal until disease onset and another with more behavior abnormalities before onset and more negative symptoms. Konstantareas & Hewitt (2001) hypothesize that the latter group may have stronger links with autism. Autism is also widely regarded as a heterogeneous condition. This suggests methods such as cluster analysis could be used to identify subgroups with related characteristics across these diagnostic boundaries.
The characteristics of samples used in these studies also limit generalizability of the findings. Samples are frequently small and exclude autistic individuals with IQs below 70 or 80 despite the increased prevalence of intellectual disability in this population. Females on the autism spectrum are under-included or even excluded from these studies even when accounting for the high male-to- female ratio in autism. This may affect study results since autism in females may be associated with a subtly different cognitive profile and characteristics than in males (Lehnhardt et al. 2016). Psychosis and related traits were also more frequently studied in autistic children and adolescents despite the fact that psychosis typically has onset in adulthood or late adolescence.
Finally, research in several relevant areas is insufficient or absent, especially studies directly comparing autism and SSD. Furthermore, few studies have investigated how much neurological and genetic traits related to bipolar disorder could account for the relationship between autism and schizophrenia, despite the fact that bipolar disorder has strong biological links with both autism (Chisholm et al. 2015; Stahlberg et al. 2004) and schizophrenia (Craddock et al. 2009). This also suggests those with schizoaffective disorder (mixed schizophrenia and bipolar-like symptoms) may be a useful comparison group. The prevalence, character and outcomes of psychotic-like traits short of full psychosis in autism is also understudied. Most of all, the majority of the research comparing these disorders has put little or no focus on the implications for treatment of those who currently have ASC or SSD.
In the future, research can be applied for more specific and accurate diagnosis of those with autistic and psychotic traits. Distressing or impairing symptoms with common etiologies can also be treated across diagnostic lines. For example, as described earlier, a screening tool designed for those psychosis was successfully applied to identify distressing perceptual abnormalities in autistic adults (Milne et al . 2017).
The research is consistent with a complex relationship between autism and schizophrenia, consistent with both overlapping and exclusive relationships in psychology, behavior and etiology. This implies that our current diagnostic classifications may be insufficient for individuals presenting with these characteristics. Disentangling these relationships can lead to a better understanding of both autism and schizophrenia spectrum conditions, which with careful application, can lead to improved functional outcomes and well-being of those labeled with autism or schizophrenia spectrum conditions.
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