There is much controversy in the realm of understanding the linkages between these conditions. As an observer, it is intuitively obvious that some people with hyper-focused Attention Deficit Disorder (ADD) seem most like a self-absorbed autistic person; and similarly that the cognitive lapses of absence epilepsy are quite similar to a very inattentive ADD patient.
In 2005, Hughes & Melyn reported: “The goal of this study was to investigate the incidence of epilepsy and also the EEG findings among children with autism, a devastating disorder, and to compare these data to an EEG control group. EEGs were quantified as to the degree of epileptiform activity and also slow wave abnormalities. Abnormal EEGs were found in 75% of the 59 children and 82% of their 151 EEGs; 46% had clinical seizures. Nearly all children with seizures had epileptiform activity, but almost 20% of those with spike discharges did not have clinical attacks. Slow wave abnormalities were more frequent and of a greater degree of severity in the group {of patients}, compared to controls.”
In 2010, Rommelse reported: “Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both highly heritable neurodevelopmental disorders. Evidence indicates both disorders co-occur with a high frequency, in 20–50% of children with ADHD meeting criteria for ASD and in 30- 80% of ASD children meeting criteria for ADHD.”
In 2011, Bennett-Black reported on the link between ADD with benign epilepsy, and compared these children to their siblings: “This prospective study explores the prevalence and characteristics of attention-deficit hyperactivity disorder in children with benign epilepsy, compared with its prevalence in their siblings. Among 40 patients with benign epilepsy, 28 (70%) were diagnosed with attention deficit hyperactivity disorder: 19 with the in-attentive type, one with the hyperactive type, and eight with the combined type. In the control group of 12 siblings, only two (16.7%) were diagnosed with attention deficit hyperactivity disorder.”
In summary, there are similarities at the level of EEG results, genetic linkage, and clinical outcome. When confronted with treatment resistance it is wise to carefully reconsider the diagnosis by evaluating at an objective or physiological level. With, and after reviewing family history, treatment planning can consider the entire person from the vantage of medical science and with respect for individual differences.
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