TPC-Journal-V5-Issue2

278 Additionally, Davies and Gavin (2007) and Gavin et al. (2011) found differences in brain activity between children with and without SPD using electroencephalography. In fact, “brain activity correctly distinguished children with SPD from children who were typically developing with 86% accuracy” (Davies & Gavin, 2007, p. 176). Finally, in a recent study ( N = 40), Owen et al. (2013) found neurological differences in brain structure between children with and without SPD, specifically stating: Children with SPD show specific reduction in the white matter microstructure primarily affecting posterior cerebral tracts. . . . These findings suggest that children with SPD have a specific imaging biomarker for their clinical disorder and the pattern of their shared structural difference. (p. 850) Significant sensory abnormalities (e.g., SPD) can be comorbid with several childhood clinical disorders such as ASD, attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, depression, Fragile X syndrome and obsessive-compulsive disorder (Ghanizadeh, 2011; Goldsmith, Van Hulle, Arneson, Schreiber, & Gernsbacher, 2006; Tomchek & Dunn, 2007; Van Hulle, Schmidt, & Goldsmith, 2011). At the same time, researchers are suggesting that SPD is a separate and distinct disorder. For example, when studying youth with ASD and SPD, Schoen et al. (2009) d emonstrated differences in sympathetic nervous system functions and sensory-related behaviors between children in the two samples, while Chang et al. (2014) reported differing patterns of brain connectivity in adolescents with the two separate diagnoses. In addition, Miller et al. (2012) studied differences between youth with SPD, ADHD and the two dual diagnoses by using several parental- report instruments and measuring physiological reactions to sensory stimuli by electrodermal response. They found that participants with ADHD had greater inattention and participants with SPD had the most sensory issues, while those with both diagnoses experienced inattention and fewer sensory issues than those who only had SPD. Further, participants with SPD had greater physiological or electrodermal reactivity to sensory stimuli than participants with ADHD (Miller et al., 2012). Overall, differences seem to exist between participants with SPD and those with similar but varying clinical diagnoses (e.g., ADHD and ASD), suggesting SPD as an individual disorder. Etiology . While the etiology of SPD is still largely unknown, several researchers believe that SPD may have a genetic basis (e.g., Goldsmith et al., 2006; Miller et al., 2009; Owen et al., 2013; Van Hulle et al., 2011). For example, Goldsmith et al. (2006) studied the tactile and auditory defensiveness, temperament, and behavior problems of toddler-aged twins as determined by parent reports. Researchers determined moderate genetic influences with tactile defensiveness, leading them to suggest more research investigating the heritability of SPD and sensory issues. Overall, although SPD is controversial, there is substantial evidence for SPD as a distinct disorder in children. According to the APA (2013), A mental disorder is a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning. Mental disorders are usually associated with significant distress or disability in social, occupational, or other important activities. (p. 20) Based on the literature review, we believe that SPD meets the APA’s criteria for a mental health disorder, due to an irregular neurological pattern of receiving, sending, processing and responding to stimuli, which results in impairment to an individual’s regular behavioral and emotional functioning. Professional counseling. SPD has received some, albeit limited recognition in the counseling field (e.g., Collier & Falls, 2010; Katz, 2006; Withrow, 2007), including an article featured in Counseling Today (Murphy,