New research suggest that the pathophysiology of ASD + ADHD may be primarily related to somatosensory deficits and delayed maturation of the left postcentral gyrus. Abnormal somatosensory, attributed to delayed maturation of the left postcentral gyrus, leads to the core symptoms experienced by patients with comorbid ASD and ADHD.
Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) share high rates of comorbidity, with the Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition now acknowledging the comorbid diagnosis of ASD and ADHD. Although structural abnormalities in the prefrontal cortex, cerebellum, and basal ganglia occur in both ASD and ADHD, no structural studies have focused exclusively on patients with comorbid ASD and ADHD. We thus aimed to clarify the structural features and developmental changes in patients with comorbid ASD and ADHD in a relatively large sample from two sites. Ninety-two patients were age-matched to 141 typically developing (TD) controls (age range: 5–16 years) and assessed for volumetric characteristics using structural magnetic resonance imaging (i.e. surface-based morphometry). While there were no significant differences in prefrontal cortex, cerebellum, and basal ganglia volumes, patients with ASD and ADHD exhibited significantly lower left postcentral gyrus volumes than TD controls. We observed significantly lower postcentral gyrus volumes exclusively in children and preadolescents, and not in adolescents. Our findings suggest that abnormal somatosensory, attributed to delayed maturation of the left postcentral gyrus, leads to the core symptoms experienced by patients with comorbid ASD and ADHD.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social impairments, communication deficits, restricted interests, and repetitive behaviours. Attention-deficit/hyperactivity disorder (ADHD), another neurodevelopmental disorder, is like-wise characterized by age-inappropriate inattention, hyperactivity, and impulsivity. The prevalence of both disorders is high, with recent reports indicating that ASD is found in 1.5% of the population, while ADHD is found in 7.2%. ASD and ADHD are more common in boys than in girls, with a male-to-female ratio of about 3–4:1. Individuals with ASD or ADHD have difficulties in daily life and often develop a variety of comorbidities such as oppositional defiant disorder, conduct disorder, depression, and anxiety disorder, especially during adolescence or later. It is therefore critical to diagnose and treat these patients early, to prevent the development of secondary psychiatric problems.
(Note: The citations are taken ‘out-of-context’ for editorial purposes only, not to misrepresent the actual text in the study. Please refer to the full text, for a complete insight).
ADHD and ASD, leading to ADHD traits in patients with ASD being largely ignored and such patients diagnosed with ASD only.
However, clinical symptoms of inattention and hyperactivity often occur in individuals with ASD, and children and adolescents with ADHD often exhibit social interaction deficits, with 28% of patients diagnosed with ASD reported to likely also have comorbid ADHD and up to 70% of patients with ADHD exhibiting ASD symptoms.
In both ASD and ADHD, effective use of stimulant medications can reduce ADHD symptoms, including hyperactivity and inattentiveness, while the behavioural symptoms of ASD remain unchanged.
These findings provide further evidence that ADHD and ASD are two distinct disorders.
Despite high comorbidity and greater impairment experienced by individuals with both conditions rather than a single diagnosis, brain imaging studies of individuals with co-occurring ADHD and ASD are limited and the underlying pathophysiology remains unclear.
While ASD is often associated with brain overgrowth in early childhood and adolescence, individuals with ADHD often exhibit smaller brain volumes.
The prefrontal cortex and basal ganglia (e.g. the caudate) exhibit increased volumes in ASD, and the same regions exhibit decreased volumes in individuals with ADHD.
In contrast, the cerebellum and the corpus callosum exhibit decreased volumes in both ASD and ADHD.
Taken together, these studies indicate that the cerebellum and corpus callosum are affected in similar ways in ASD and ADHD, while findings on total brain, prefrontal cortex, and basal ganglia volumes have shown opposite patterns in the two diseases.
How brain volumes are affected in patients with comorbid ASD and ADHD remains unclear.
Interestingly, children with comorbid ASD and ADHD reportedly experience more sensory processing problems than those with either ASD or ADHD alone, and postcentral gyrus abnormalities may further reflect this increased risk for sensory processing deficits.
Furthermore, sensory processing abnormalities contribute to social, communication, and repetitive behaviour deficits, which are the core features of ASD and are also associated with attentional deficits.
Therefore, in children with comorbid ASD and ADHD, sensory problems may stem from postcentral gyrus abnormalities, which in turn may lead to core ASD and ADHD symptoms (social, communication, repetitive behaviour, and attentional deficits).
There were no significant differences in total intracranial, total grey matter, total cortical, subcortical grey matter, or cerebellum cortex volumes between the two groups (Table 1S).
Similarly, there were no significant differences in the volumes of the basal ganglia, such as the nucleus accumbens, amygdala, caudate, hippocampus, pallium, putamen, and thalamus (Table 2S).
This finding suggests that ASD and ADHD are neither phenocopies nor additive pathologies, but that comorbid ASD and ADHD represents a distinct neurofunctional pathology altogether.
In the present study, we assessed the unique brain structure features of patients with ASD + ADHD. This approach, to the best of our knowledge, has not been used elsewhere, and the relatively large sample size used here presents a significant advantage. Patients with ASD + ADHD exhibited significantly decreased left postcentral gyrus volumes compared to TD controls; however, the left postcentral gyrus volume in patients with ASD + ADHD was only significantly smaller in children and pre-adolescents, not in adolescents. These findings suggest that the pathophysiology of ASD + ADHD may be primarily related to somatosensory deficits and delayed maturation of the left postcentral gyrus. Our results improve the field’s current understanding of the neurobiological mechanisms underlying comorbid ASD and ADHD and may lead to the development of novel treatment strategies that consider the relevant pathophysiology.
Mizuno, Y., Kagitani-Shimono, K., Jung, M., Makita, K., Takiguchi, S., Fujisawa, T. X., Tachibana, M., Nakanishi, M., Mohri, I., Taniike, M., & Tomoda, A. (2019). Structural brain abnormalities in children and adolescents with comorbid autism spectrum disorder and attention-deficit/hyperactivity disorder. Translational psychiatry, 9(1), 332. https://doi.org/10.1038/s41398-019-0679-z
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