What is the difference between childhood schizophrenia and autism

Clinician judgments about diagnoses were informed by a variety of information, including clinician interactions with participants during administration of diagnostic assessments and prior psychiatric and medical histories obtained during recruitment procedures. This decision was made to ensure ability to accurately self-report during diagnostic assessments. TD participants were excluded if they had any history of a psychiatric diagnosis or if they had immediate family members with an ASD or SZ diagnosis.

All participants provided their written informed consent to participate in this study in accordance with the Declaration of Helsinki. It is commonly used in ASD research to confirm diagnoses in a standardized manner and to estimate the severity of ASD traits The ADOS-2 algorithm sums across a subset of scored items in order to categorize participants into autism representing higher severity ASD traits , autism-spectrum representing lesser severity of ASD traits, but still enough to constitute ASD criteria , and non-spectrum.

The positive symptom scale assesses the presence of delusions, conceptual disorganization, hallucinatory behavior, excitement, grandiosity, suspiciousness, and hostility. Although the PANSS is intended to inform clinician judgment in considering severity of current psychosis symptoms, there are no diagnostic cut-off scores. The PANSS also has a General Psychopathology scale that measures somatic concerns, anxiety, and depression among other symptoms, but this scale was not analyzed for the purposes of the present study.

As reported in Table 2 , sensitivity refers to the percentage of participants with ASD who met the ADOS-2 criteria for either autism or autism-spectrum. ROC curves offer similar sensitivity and specificity information but differ in that, instead of using algorithm cut-off scores as in Table 2 , ROC curves examine the extent to which continuous ADOS scores correctly classify participants into DSM-5 diagnostic categories. Areas under the curve AUC of 1 represent perfect sensitivity and specificity of a measure, whereas.

All analyses on diagnostic accuracy are based on the ADOS-2 algorithm cut-off scores and the subset of items that comprise this algorithm. Examples of negative items include absence or diminished observation of typical behaviors such as absence of descriptive or instrumental gesture, deficient reporting of events, lack of communication of affect, or absence of social overtures.

Six ADOS items that could not easily be categorized as positive or negative e. We then examined the ROC curves of the positive and negative scales we created to examine their functioning in discriminating diagnostic groups. These analyses were conducted to check whether the pattern of the main findings from the primary analyses was confounded by group differences in IQ and sex.

Of particular interest for the present study was a high rate of false positives in SZ, yielding a specificity of Seventeen out of 39 participants The AUC for the entire sample was.

For both analyses, tests for homogeneity of variances were violated. Therefore, we ran Brown——Forsythe tests to examine equality of means and Games—Howell post hoc comparisons, which are more robust to homogeneity of variance violations.

Diagnosis had a statistically significant effect on both positive symptoms, F 2, Therefore, we ran Brown—Forsythe tests to examine quality of means and Games—Howell post hoc comparisons, which are more robust to homogeneity of variances violations.

Diagnosis had a statistically significant effect on both positive SZ symptoms, F 2, Error bars represent standard error of the means. Schizophrenia; TD, Typical Development. These analyses suggest that the key findings from our analyses were unlikely to be confounded by sex or IQ. The key aim of this study was to examine the utility of ASD and SZ diagnostic instruments in discriminating these respective disorders. These findings are similar to those of Bastiaansen, Meffert 43 who found that ADOS-2 algorithm totals 44 did not significantly discriminate ASD and SZ groups in their sample, which the authors suggested was due largely to behavioral overlap between negative ASD and SZ symptoms [see also 45 ].

A pattern emerged such that individuals with ASD and SZ have overlap in the overt presentation of negative symptoms, such as reduced social—emotional reciprocity, blunted affect, reduced nonverbal communication, apathy, reduced affect sharing, and reduced social overture and response, resulting in elevated scores in both groups on the negative scales of both the ADOS-2 and PANSS. Those with SZ demonstrated higher positive symptoms related to psychosis e.

Few positive ASD symptoms were noted in SZ patients, suggesting that ratings of these symptoms may be most helpful in making a differential diagnosis in this context. This was the first time that negative and positive ASD symptoms have been split apart within a clinical measure of ASD symptoms and doing so seems to improve sensitivity and specificity. There are two key clinical implications of this study, both related to situations where clinicians are considering a differential diagnosis between SZ and ASD.

Second, in order to resolve this confusion, clinicians ought to focus on the presence or absence of positive symptom domains of both ASD and SZ. Positive symptoms, especially hallucinations, delusions, grandiosity and suspiciousness may be most indicative of SZ. On the other hand, positive symptoms related to odd or excessive emotional gestures, echolalia, stereotyped speech patterns, unusual mannerisms, or circumscribed interests may be most indicative of an ASD diagnosis.

Evidence of positive symptoms from both ASD and SZ diagnostic assessments may warrant a dual diagnosis, which recent research converges in suggesting occurs with more frequency than once thought 27 , Findings from this study also call for increased research into the shared underlying biological systems that may give rise to ASD and SZ. Across both measures of ASD and SZ symptoms, individuals from both diagnostic categories earned elevated negative symptom scores. Previous research has identified parallel deficits in social cognition in ASD and SZ 37 that may have similar origins in atypical neural activation of select brain areas There is a need for further research to understand whether the mechanisms contributing to negative symptoms in ASD and SZ are shared or distinct.

Indeed, despite similar deficits in facial emotion recognition in ASD and SZ, there are markedly different patterns of EEG- and fMRI-measured neurological dysfunction associated with these deficits 46 , Moreover, some have questioned whether negative symptoms in schizophrenia are primary e. Resolving the matter of whether negative symptoms have similar or distinct biological mechanisms is critical for determining whether ASD and SZ populations are likely to benefit from similar treatments.

Likewise, better understanding the neural mechanisms of more distinct positive features of SZ and ASD may provide clues to disorder-specific pathology that could be helpful for understanding etiology, distinguishing between disorders, and developing targeted treatment. Future research on this topic would benefit from measures that are a priori designed to categorize ASD symptoms into positive and negative symptoms similar to what is common practice for measuring SZ symptoms on instruments like the PANSS used in the present study.

Many items on existing ASD measures do not clearly differentiate between positive and negative symptomology. In our analysis with the ADOS-2, there were 11 items where one or more of the codes could not be categorized as either positive or negative. In this example, the first individual displays the absence of a typical behavior negative symptom , whereas the second displays the presence of an atypical behavior positive symptom.

However, the rating on the ADOS-2 item as currently written is identical. As such, there is an unfortunate missed opportunity here to dissociate potentially clinically and biologically meaningful differences in behavior see Supplemental Material for other ADOS-2 examples.

Similar to what is already common practice in SZ research, the distinction between positive and negative symptoms may be useful for parsing heterogeneity within the ASD population, for better understanding the biology of distinct symptom manifestations and for targeting treatment. Instruments better designed to capture symptoms along these dimensions would move this goal forward.

Limitations of this study include the small sample size and unequal sex and IQ among the different diagnosis groups. While statistically controlling for sex and IQ did not change the overall pattern of results, it would have been more ideal if all groups were equal on these participant characteristics. Indeed, others have delineated the importance of carefully considering how IQ affects the results of ADOS-2 assessments However, our IQ range was relatively typical of SZ samples, and lesser cognitive impairment in adults with ASD compared to SZ may more accurately represent these respective populations Another limitation is that the ADOS-2 Positive and Negative items were derived post hoc and without a separate validation study, and many ADOS-2 items describing core ASD features could not be classified as either positive or negative so are omitted from our scales.

We are not advocating for the use of the subscales we created for diagnostic purposes. A final limitation is that, paralleling clinical activity in ASD and SZ, this study was not supported by neuroimaging, electroencephalography, or genetic data. Future research is needed to determine the biological systems that distinguish positive and negative symptom domains across ASD and SZ. In spite of these limitations, this study has important findings adding to a body of literature demonstrating substantial symptom overlap between adults with ASD and SZ.

While positive and negative SZ symptoms have long been discussed and measured in the schizophrenia literature, this study shows for the first time that distinguishing positive and negative SZ symptoms in ASD has unique value.

The findings also point to the need for supplemental diagnostic measures that could more effectively parse symptom heterogeneity in ASD and better distinguish other disorders like SZ.

Additional work exploring the biological overlap between ASD and SZ, as well distinguishing positive symptoms of each disorder is clearly warranted. Data used in the preparation of this manuscript are publicly available to approved researchers as part of the NIMH Data Archive nda.

DT analyzed the data and wrote the bulk of the manuscript. JF-F helped design and conceptualize the study, assessed participants, and wrote and edited sections of the manuscript. AN helped with statistical analysis and reviewed drafts of the paper.

AA and VS were involved with conceptualization of the study, participant recruitment and assessment. Both groups are known to be poor at recognizing social cues. They often have difficulty identifying emotion in other people, so their reactions may seem inappropriate. By not picking up on the subtle cues in interactions, adults with ASD or schizophrenia may alienate other people and have trouble making friends or getting along with classmates or co-workers.

Along with collaborators at Southern Methodist University, Sasson is conducting new research at the UT Dallas Callier Center for Communication Disorders that compares the basis for social interaction impairments between adults with ASD and adults with schizophrenia.

He is attempting to understand the mechanisms that underlie their social limitations. What works well for individuals with ASD might be very different than those with schizophrenia. In previous research, Sasson and his colleagues used eye-tracking technology and found that neither adults with ASD nor adults with schizophrenia look at social information in the same way as those without either disorder.

His colleagues also found that parts of the brain that process social information are underactive in those with ASD and schizophrenia. But the researchers have also found differences. Individuals with ASD do not spontaneously orient to emotional information, while individuals with schizophrenia do. While both groups show aspects of paranoia in social situations, Sasson and his colleagues are discovering that the root cause of the paranoia is different for each disorder.

By differentiating between schizophrenia and autism, and by examining how patients react in social settings, Sasson said he hopes researchers can develop new ways to counteract the negative social experiences of patients. This prepsychotic developmental disorder includes deficits in communication, social relatedness, and motor development, similar to those seen in autism spectrum disorders ASD.

Autism and schizophrenia may present as 2 separate disorders that need to be differentiated, or as comorbid conditions. It is important to remember that some individuals may have both COS and ASD, which has implications when designing appropriate biopsychosocial interventions. Adult psychiatrists may benefit from additional training in the diagnosis of ASD in adults, whereas child psychiatrists may benefit from increased comfort with identifying primary psychotic symptoms in autistic youth.

The diagnosis had initially been made when George was 27 months old and had been reconfirmed by numerous well-regarded autism experts over the years.

George had received the usual autism-specific services, and although he made gains, he continued to present with atypical behaviors. George was referred to Dr Frazier because of an increase in the intensity and frequency of unusual and disturbing preoccupations that often had a morbid theme.

Those who worked with him had difficulty in getting him off of these disturbing topics. George also had unusual behaviors and mood-regulation difficulties. Initially, these friends were humming to him or saying hello. Because of a history of at least 1 depressive episode and what appeared to be more of a chronic euphoric state with affective lability, George was given a provisional comorbid diagnosis of bipolar disorder with psychotic features.

Over the ensuing years, despite a number of medication trials including atypical antipsychotics and mood stabilizers, he became tortured by more persistent auditory hallucinations. His comorbid diagnosis was changed to schizoaffective disorder and, more recently, to schizophrenia. He is currently taking a typical antipsychotic.

These symptoms, present since early childhood, predated his symptoms of psychosis and continue to require the support of autism-specific services. Although epidemiological studies of the genetic relationship between autism and schizophrenia are deficient, evidence does exist for shared genetic factors.

Copy number variant and rare allele studies have found a relationship between autism and point and structural mutations in neurologins, neurexins, and related genes. There have also been reports that implicate the neurexin family in schizophrenia.

Neurologins are a family of postsynaptic proteins that bind transsynaptically to neurexins, which are presynaptic proteins that seem necessary for both excitatory and inhibitory synaptogenesis and synapse maturation. This fits with the neurodevelopmental insult and imbalance in excitatory and inhibitory transmission hypothesis for both autism and schizophrenia.

Specific deletions associated with schizophrenia include 22q Both autism and schizophrenia have accelerated trajectories of brain development around the age of symptom onset: those with autism have an acceleration or brain overgrowth during the first 3 years of life, and those with COS have an acceleration of brain development pruning during adolescence. Cheung and colleagues 25 attempted to quantify brain structural similarities and differences in ASD and schizophrenia using a quantified anatomical likelihood estimation approach to synthesize existing brain imaging datasets.

Using this model, they extracted foci from 25 voxel-based studies comprising patients ASD, first-episode schizophrenia and controls. Those with ASD and schizophrenia had lower gray matter volumes within limbic-striato-thalamic neurocircuitry than did controls.

Unique features included lower gray matter volume in the amygdala, caudate, and frontal and medial gyrus for schizophrenia, and lower gray matter volume in the putamen for autism. The researchers concluded that in terms of brain volumetrics, ASD and schizophrenia have a clear degree of overlap that may reflect shared etiological mechanisms. A variety of psychosocial and educational interventions that support children with COS and children with ASD exist to address core deficits in socialization, communication, and behavior and the associated developmental and medical conditions.

A thorough description is beyond the scope of this article, however. Atypical antipsychotics are the mainstay of pharmacotherapy for schizophrenia at any age, and they have also been used to manage certain symptoms, particularly irritability, associated with ASD.

Developmental delays are described premorbidly in samples of children and adults with schizophrenia. More recently, the notion that ASD and schizophrenia can present comorbidly in a subset of patients has received further attention in the literature.

The differential diagnosis between these disorders and the comorbid diagnoses of the two conditions is often a bit of a quagmire for clinicians. We see children with ASD who have emerging psychotic symptoms. In these children, the hallucinations or delusional preoccupations may initially be attributed to the developmental disorder. Conversely, we also see adolescents or young adults with schizophrenia who have a developmental history consistent with ASD typically higher functioning and who continue to have comorbid ASD.

Yet some have not previously received a diagnosis of ASD. Adult psychiatrists and mental health professionals would benefit from further training in the diagnosis of ASD in adults, and child mental health professionals would benefit from training in the diagnosis of schizophrenia spectrum disorders in youths. Given the complex symptom profile in youths with schizophrenia spectrum disorders, there tends to be a delay in diagnosis, even when symptoms are present for years.