**5.1 Brain dysfunction in children with autism spectrum disorders**

Autism spectrum disorders (ASDs), including autistic disorder and Asperger disorder, are diagnosed by cataloguing behavioural features including the impairment of reciprocal social interaction and communication, as well as the presence of repetitive ritualistic behaviour or interests. Methodological differences make it difficult to compare epidemiological studies; therefore, there are discrepancies in the reported prevalence of ASDs. However, the prevalence of ASDs has been conservatively estimated at 36.4/10,000 (Fombonne, 2005). The severity of impairment varies greatly among patients, and they occasionally show mental retardation. The impairment is evident at least prior to the age of 3 years, and its effects persist life-long.

ASDs are characterised by pervasive impairments in social behaviour. Accumulating evidence suggests that adults with ASDs have altered brain activity in regions related to social interactions (Neuhaus et al., 2010), such as the superior temporal gyrus (Meresse et al., 2005), fusiform gyrus (Koshino et al., 2008), amygdala (Pinkham et al., 2008), and prefrontal cortex (Gilbert et al., 2009). Although previous studies have elucidated that adults with ASDs show reduced or altered activation in the aforementioned regions compared with healthy adults, surprisingly, little neuroimaging data are available for autistic children.

Kawakubo et al. examined prefrontal haemodynamic activation during a verbal fluency task in children and adults with ASDs (Kawakubo et al., 2009). In children, there were no significant differences in the haemodynamic changes between patients with ASDs and healthy controls. However, the concentration of oxy-haemoglobin in adults with ASDs was

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significantly lower than that in healthy controls. These findings suggest that developmental changes in prefrontal activity of individuals with ASDs emerge before adulthood, i.e. they appear during adolescence.

## **5.2 Brain dysfunction in children with attention-deficit hyperactivity disorder**

Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder whose prevalence has been estimated to be 3% to 7% of school-age children (American Psychiatric Association [APA], 2000). The essential clinical symptoms include inattention and/or hyperactivity-impulsivity. Some hyperactive-impulsive or inattentive symptoms must be present before the age of 7 years, although some symptoms that cause impairment tend to persist life-long. Some impairment from the symptoms is typically evident at school and at home, with behaviour that is clearly inappropriate for the developmental age in social, academic, or occupational settings.

In particular, ADHD is characterised by impairments in executive function, i.e. the failure of inhibitory control and the dysregulation of brain systems mediating reward and response (Sonuga-Barke, 2003). The Go/NoGo task, stop-signal task, and Stroop colourword task have been used to investigate the inhibition process in these patients. Some studies have examined brain function in ADHD children during the Stroop colour-word task using NIRS. Moser et al. examined the brain activation in the dorsolateral prefrontal cortex (Moser et al., 2009), and showed that the oxy-haemoglobin concentration peaked later in ADHD children than in healthy children. Additionally, the concentration of deoxy-haemoglobin increased just after the onset of stimulation in ADHD children but decreased in healthy children. Negoro et al. examined the activation of frontal regions in the brain using 24-channel NIRS during the Stroop colour-word task (Negoro et al., 2010), and showed that the concentration of oxy-haemoglobin in the inferior prefrontal cortex in ADHD children decreased compared with that in healthy children, especially in the both the inferior lateral prefrontal cortex.

The trail-making test, which assesses executive function, has been used for the measurement of brain activation in ADHD children. Weber et al. showed that the concentration of oxyhaemoglobin increased in ADHD children during the short attention phase, whereas no significant change was observed in healthy children (Weber et al., 2005). A significant increase in oxy-haemoglobin was also reported for both groups during the extended attention phase, although an additional increase was observed in deoxy-haemoglobin level only in the healthy children.

These findings suggest that during tasks involving executive function, the haemodynamic responses in ADHD children are different from those in healthy children.
