F or the past two decades, researchers have consistently identified a pattern of neurocognitive deficits (e.g., attention/concentration difficulties and deficits in executive functioning) in many childhood cancer survivors that may significantly impact their academic performance, social/interpersonal relationships, and vocational success if left unidentified or untreated. As such, it is imperative that researchers focus on understanding the specific nature of these deficits, their precise etiology, and efficacious treatment approaches. To better understand the nature of these deficits, a number of research teams have used an attention-deficit/hyperactivity disorder (ADHD) conceptual framework to guide their research efforts. Findings suggest that indeed many childhood survivors of leukemia [1] and brain tumors [2] evidence attentional difficulties consistent with the inattentive subtype of ADHD. In this issue of Pediatric Blood & Cancer, Kahalley et al. further explore rates of occurrence of ADHD and secondary ADHD (SADHD) in pediatric cancer survivors and compare those rates to that in the general population. The term SADHD refers to an ADHD-like presentation acquired from a non-developmental presentation, such as a traumatic brain injury, or for the purposes of their research, neuro-toxic cancer treatments. Importantly, they conclude that the clinical presentation of cancer survivors does not resemble that of either ADHD or SADHD, and suggest that the current DSM-IV diagnostic criteria and nomenclature may not characterize the types of deficits that pediatric cancer survivors manifest. We would like to underscore the problems in utilizing a classic, developmental ADHD framework for understanding cognitive late effects in childhood cancer survivors, and argue that there are inherent theoretical and clinical shortcomings to this approach. Our first theoretical concerns center on the issue of diagnostic specificity. Identification of SADHD as a potential diagnosis in pediatric cancer survivors that only differs from conventional/premorbid ADHD with regard to etiology and onset, ignores the very characteristics that distinguish ADHD from other childhood disorders. That is, age of onset, pervasiveness, and impairment are particularly important in discriminating ADHD from other childhood disorders, given the characteristic symptoms of ADHD are not pathognomic. For example, attention difficulties are frequently associated with almost all diagnoses of childhood. Children with anxiety or mood disorders are often restless, fidgety, and may struggle to attend to class lectures due to the interference of persistent ruminations. Racing thoughts, pressured speech, and/or delusions associated with early onset bipolar disorder are expected to create similar interference with attentional processes, while children with autism spectrum disorders are frequently described as ‘‘being in their own world.’’ To sum, it is illogical to conclude that an ADHD framework should be invoked simply because a similar cluster of symptoms are evident in childhood cancer survivors. A second concern revolves around the issue of etiological differences and underlying cognitive processes. Neurological correlates of developmental ADHD-related deficits include the pre-frontal and frontal cortices, basal ganglia [3], and dopaminergic and noradrenergic systems [4]. Strong evidence of ADHD as a neurological disorder may mislead researchers to conclude damage to an associated brain region secondary to intrathecal chemotherapy, radiation, and/or surgery would result in the same disorder. This fails to consider the unique developmental trajectory and underlying core processes associated with developmental ADHD, as well as potential differences in neural plasticity. Within the last few decades, executive functions such as behavioral inhibition [5] and working memory [6], have been increasingly identified as potential core deficits of ADHD. Affected children with a diagnosis of SADHD are expected to exhibit similar executive function deficits if SADHD is a comparable disorder. To date, relatively few studies have examined the effect of acute lymphocytic leukemia and/or interferon-alpha and chemotherapy treatments on executive functions, and findings have been relatively equivocal [7], and/or based on parent ratings scales rather than rigorous experimental/ neuropsychological methods. Importantly, studies indicate that the phenotype of developmental ADHD changes over time such that affected individuals tend to exhibit fewer problems related to hyperactivity in adulthood [8]. This finding likely reflects that ADHD results from delayed maturation of cortical areas involved in motor control and attention, and treatments modalities often change (e.g., change from MPH to Adderal) according to changes in symptoms. It is not clear if childhood cancer survivors exhibit a similar change in their symptoms over time, particularly since the etiology is a traumatic insult to their brain (e.g., chemotherapy), rather than a complex interaction of genetics and environmental influences. Recent studies of the Cogmed working memory training reveal promising findings that suggest the neural plasticity of children
Search from 250 M+ research papersSearch from 250 M+ research papers
Open Access
May 1, 2020
Megan E Narad + 7
