Birgit Olsson Lecture 2015
Professor Joseph Biederman's lecture "Current Concepts in the Neurobiology of ADHD Across the Lifecycle"
About Professor Joseph Biederman
Joseph Biederman is Professor of Psychiatry at the Harvard Medical School and Director of Pediatric Psychopharmacology Unit, Massachusetts General Hospital. Professor Joseph Biederman is the most cited researcher in the field of ADHD and has published over 700 scientific papers. His research in ADHD and other psychiatric disorders, including bipolar disorder, autism spectrum disorders and eating disorders, covers a variety of areas including treatment, neuroimaging, and genetics in childhood, adolescence and adult life.
"Current Concepts in the Neurobiology of ADHD Across the Lifecycle"
Current Concepts in the Neurobiology of ADHD Across the Lifecycle was the title of this year’s Birgit Olsson lecture, the fifth to date, which took place on November 18th in the Wallenberg hall in Gothenburg. This year the lecture was given by Joseph Biederman, who is a professor of psychiatry at Harvard Medical School, as well as chief of the Pediatric Psychopharmacology Unit at Massachusetts General Hospital. Professor Biederman has published more than 700 scientific articles, primarily in the field of ADHD. The prevalence of ADHD is 5-10% regardless of one’s location in the world. ADHD is at least twice as common among boys as it is among girls. The biggest problem concerning ADHD today, according to Professor Biederman, is maintaining continuity in treatment, referring to how 80-90% of all cases no longer take their medicine by one year after the start of treatment. Another problem is that there is on average a delay of almost five years from the initial onset of ADHD symptoms to the time that treatment is initiated. Joseph Biederman made a point of stressing how important these years are in a child’s life and how one can never recover these lost years, “The train of childhood passes the station only once in life”. The child’s ADHD symptoms change over time and are dependent on which context the child is in; when playing computer games they often function quite well, but when doing something they are not interested in, they function rather poorly. ADHD in girls is often overlooked and the reason for this may be that girls are less aggressive and less disruptive compared to boys. ADHD symptoms in the form of overactivity and impulsiveness often diminish after the age of twelve. Impulsiveness is usually the symptom most closely linked to poor outcome, while inattention is the symptom which most often tends to remain throughout life. In adult years, there are 15% who are no longer bothered by any ADHD symptoms, while 70% continue to have symptoms that cause some kind of disability. Adult ADHD occurs in around 5% of the population. Joseph Biederman presented three neurobiological hypotheses about ADHD; the first one concerned brain imaging. MRI studies from the beginning of the 21st century showed that individuals with ADHD had neuroanatomical anomalies in the form of significantly lower volumes in the dorsoanterior cingulate, anterior cingulate, frontal lobe and cerebellum. Studies of the width of the cerebral cortex in adults with ADHD have shown significantly thinner width in the anterior cingulate. Functional MRI of adults with ADHD has shown that the cerebral cortex in dorsoanterior cingulate is not activated in cognitive testing situations, which it is, however, for healthy comparison subjects. Other parts of the brain are activated instead in cases of ADHD. An improvement can be discerned upon treatment with methylphenidate, a psychostimulant (PS) medication, in the sense that this causes the right area to be activated. Meta-analyses have found that the volume of the basal ganglia is reduced in cases of ADHD. However, treatment with PS causes this volume to approach normal levels. The other neurobiological hypothesis concerned neurotransmitters in the form of catecholamines, where dopamine (DA) and noradrenaline are involved in ADHD. The frontal lobe cortex, which is very significantly involved in ADHD, is also the locus where dopaminergic medications such as PS have their effect. The third hypothesis concerned genetics. These days, through the help of meta-analyses, we know that ADHD, to a 75% degree, can be explained by genetic circumstances. This is a very high number compared to many other psychiatric and somatic syndromes. Candidate gene analyses have focused on the DA metabolism, and the results say that, the genes that code for the release of DA, DA receptors, as well as the transporter of DA, are all involved in ADHD in the sense that the supply of DA is reduced. In so called “genome wide association studies” (GWAS), samples from thousands of people are needed in order to be able to find a number of abnormalities on genes, which are overrepresented among people with ADHD. One of the non-genetic causes of ADHD includes, for example, when the mother smokes during the pregnancy. Animal studies, in which the mother has received nicotine while pregnant, have demonstrated that the children eventually tend to display overactive behavior regardless of gender. Psychiatric comorbidity in ADHD was the next topic on the agenda, where Biederman pointed out that PS medication often has a protective effect against comorbidity. As for substance-related syndromes, there is a critical window between the ages of 18 and 20 during which potential substance abuse problems are most likely to develop. Biederman explained that this is due to the fact that young adults often move away from home around this age and are rarely getting any ADHD medication at the time. Medication makes it less likely for people with ADHD to start smoking, and also reduces the risk that they will commit criminal acts. Having ADHD also entails an increased risk of eventually developing both posttraumatic stress syndrome and traumatic brain injuries. After the lecture, many questions were asked by those in attendance at the auditorium.