January 18, 2022
OptumLabs Data Warehouse maintains a very large database of enrollment records for U.S. commercial health insurers, as well as medical and pharmacy claims related to those clients.
A team of Mayo Clinic researchers accessed that database to examine a nationwide cohort of children born from 2006 through 2012, and who had continuous insurance coverage for at least four years from birth. In the analysis of psychiatric comorbidities and ADHD treatment in the first year after initial diagnosis, only children with at least a year of insurance coverage beyond the ADHD diagnosis were included.
The resulting cohort comprised almost a quarter-million (238,011) children, 49% of whom were girls. The racial/ethnic composition was 72.7% White, 9.8% Hispanic, 6.7% Asian, 6.2% Black, and 4.6% other or unknown.
About 5% of the children who had a diagnosis of ADHD have been made by pediatricians, with the remainder primarily by psychologists, family practice providers, psychiatrists, and neurologists. ADHD diagnoses conformed to standards set in the ninth or tenth revisions of the International Classification of Diseases (ICD-9, ICD-10).
Rates of diagnosis in the U.S. Midwest and West significantly trailed rates in the Northeast and South. Rates also rose steadily with lower household incomes, with children in households with under $40,000 annual incomes being 57% more likely to be diagnosed with ADHD than those with household incomes over $200,000.
After adjusting for sex, region, and household income, Black children were 17% less likely to be diagnosed with ADHD, relative to White children. Hispanic children were 23% less likely to be diagnosed, other/unknown children 27% less likely, and Asian children a staggering 52% less likely.
Both before and after diagnosis of ADHD, Asian children were between two and three times as likely as any other children to be diagnosed with an autism spectrum disorder. White children were more likely to be diagnosed with anxiety disorders. There were no significant differences in the frequency of depressive disorders, disruptive disorders, or oppositional defiant disorder.
After adjusting for sex, census region, and annual household income, White children were also significantly more likely to receive treatment within the first year following diagnosis of ADHD. Black children were 21% less likely to receive treatment, other/unknown children 31% less likely, and Hispanic and Asian children just over half as likely.
The authors noted, “The cause of the disparities in ADHD diagnosis according to race and ethnicity is not fully understood.†They thought it “likely that patients’ concerns about racism play some role in influencing their willingness to approach the healthcare system.†Furthermore, “Health care professionals may also contribute to the racial disparities in diagnosis and treatment. Stereotypes and bias, both explicit and implicit, have been increasingly recognized as factors potentially contributing to physicians’ clinical decision-making. It is possible, for example, that identical behavior displayed by Black and non-Hispanic White children may be interpreted differently based on race-based expectations for the behavior of children, and thus, behavior that is identified as disordered in White children might be inappropriately interpreted as normal in Black children.â€
They concluded, “Future study is needed to elucidate the mechanism behind these disparities. Clinicians should provide racially and culturally sensitive care in the evaluation and treatment of ADHD to ensure all children receive appropriate care.â€
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Parkinson’s disease is a chronic, progressive neurological disease, characterized by the drastic reduction of dopamine transporters and the dopaminergic neurons upon which they are expressed. The resulting symptoms include bradykinesia (slowness of initiation of voluntary movements), tremors, rigidity, and postural instability.
Taiwan’s National Health Service covers about 99 percent of its 24 million inhabitants, and maintains complete records in its National Health Insurance Research Database. The Longitudinal Health Insurance Database2000 (LHID 2000) is a nationally representative subset of the latter.
Using the LHID 2000, a Taiwanese research team identified10,726 patients with Parkinson’s disease. It paired them with an identical number of randomly selected non-Parkinson’s controls, matched by age, gender, and index date (first date of diagnosis of Parkinson’s disease).
The team then looked retroactively through the database to determine which of the 21,452 individuals had previously been diagnosed with ADHD. Fourteen of the 10,726 Parkinson’s patients had been diagnosed with ADHD, versus five of the 10,726 in the control group.
Parkinson’s patients were thus 2.8 times as likely to have had a previous diagnosis of ADHD as the controls. When adjusted for age, gender, and Carlson Comorbidity Index scores, they were 3.6 times as likely to have had a previous ADHD diagnosis.
The authors cautioned that this association between prior ADHD diagnosis and subsequent Parkinson’s diagnosis is not causal.
Only one in 766 of Parkinson’s patients (a seventh of one percent) had previously been diagnosed with ADHD. So even if there were any causal relationship, it would be extremely weak.
Sleep disorders are one of the most commonly self-reported comorbidities of adults with ADHD, affecting 50 to 70 percent of them. A team of British researchers set out to see whether this association could be further confirmed with objective sleep measures, using cognitive function tests and electroencephalography (EEG).
Measured as theta/beta ratio, EEG slowing is a widely used indicator in ADHD research. While it occurs normally in non-ADHD adults at the conclusion of a day, during the day it signals excessive sleepiness, whether from obstructive sleep apnea or neurodegenerative and neurodevelopmental disorders. Coffee reverses EEG slowing, as do ADHD stimulant medications.
Study participants were either on stable treatment with ADHD medication (stimulant or non-stimulant medication) or on no medication. Participants had to refrain from taking any stimulant medications for at least 48 hours prior to taking the tests. Persons with IQ below 80 or with recurrent depression or undergoing a depressive episode were excluded.
The team administered a cognitive function test, The Sustained Attention to Response Task (SART). Observers rated on-task sleepiness using videos from the cognitive testing sessions. They wired participants for EEG monitoring.
Observer-rated sleepiness was found to be moderately higher in the ADHD group than in controls. Although sleep quality was slightly lower in the sleepy group than in the ADHD group, and symptom severity slightly greater in the ADHD group than the sleepy group, neither difference was statistically significant, indicating extensive overlap.
Omission errors in the SART were strongly correlated with sleepiness level, and the strength of this correlation was independent of ADHD symptom severity. EEG slowing in all regions of the brain was more than 50 percent higher in the ADHD group than in the control group and was highest in the frontal cortex.
Treating the sleepy group as a third group, EEG slowing was highest for the ADHD group, followed closely by the sleepy group, and more distantly by the neurotypical group. The gaps between the ADHD and sleepy groups on the one hand, and the neurotypical group on the other, were both large and statistically significant, whereas the gap between the ADHD and sleepy groups was not. EEG slowing was both a significant predictor of ADHD and of ADHD symptom severity.
The authors concluded, “These findings indicate that the cognitive performance deficits routinely attributed to ADHD … are largely due to on-task sleepiness and not exclusively due to ADHD symptom severity. … we would like to propose a simple working hypothesis that daytime sleepiness plays a major role in cognitive functioning of adults with ADHD. … As adults with ADHD are more severely sleep deprived compared to neurotypical control subjects and are more vulnerable to sleep deprivation, in various neurocognitive tasks they should manifest larger sleepiness-related reductions in cognitive performance. … One clear testable prediction of the working hypothesis would be that carefully controlling for sleepiness, time of day, and/or individual circadian rhythms would result in a substantial reduction in the neurocognitive deficits in replications of classic ADHD studies.”
Neurofeedback, also known as EEG (electroencephalogram)biofeedback, is a treatment that seeks to alleviate symptoms of various neurological and mental health disorders, including ADHD. It does this through immediate feedback from a computer program that tracks a client’s brainwave activity, then uses sound or visual signals to retrain these brain signals. This in principle enables patients to learn to regulate and improve their brain function and reduce symptoms.
An Iranian study team recently performed a systematic search of the peer-reviewed medical literature. It identified seventeen randomized-controlled trials (RCTs) of neurofeedback treatment for children and adolescents with ADHD that could be aggregated for meta-analysis.
A meta-analysis of twelve RCTs with a combined total of 740 youths looked at parent ratings of changes in hyperactivity/impulsivity symptoms, and separately of changes in inattention symptoms. In both instances, the net pooled effect centered on zero.
A meta-analysis of nine RCTs with a combined total of 787 youths examined teacher ratings. Once again, the pooled change hyperactivity/impulsivity symptoms centered on zero. For inattention symptoms, the teacher ratings centered on a tiny improvement, but it did not approach statistical significance. The 95% confidence interval stretched well into negative territory.
There was no sign of publication bias. Between-study heterogeneity, on the other hand, was high, with some small sample size RCTs pointing to reduced symptoms, and other small sample size RCTs pointing to increased symptoms. However, the RCTs with the larger sample sizes clustered close around zero effect size.
The authors concluded, “The results provide preliminary evidence that neurofeedback treatment is not an efficacious clinical method for ADHD.â€
