With ADHD, the brain is wired differently!

Following on from a blog we posted last November, about the role of mother’s Vitamin D intake during gestation and its relationship to the occurrence of ADHD in the child, this post explores research into what is going on in the brain of the child with ADHD.

In order to unpack the anatomy of the brain, researchers use structural imaging, such as computed tomography (CT) scans and magnetic resonance imaging (MRI) to capture two- or three-dimensional images, which are used to determine the size and volume of the whole brain or specific areas within the brain.

For investigating the functions of the brain, researchers use scans that show activity within the brain. The earlier types of functional scans, such as electroencephalography (EEG) and single-photon emission computed tomography (SPECT), measured patterns of nerve activity or blood flow, respectively. More recent methods, such as positron emission tomography (PET), use radioactive tracers that can be seen in the brain.

Most of what is known about dopamine function in the brain has been gleaned from the use of a radioactive tracer, raclopride, which is injected into the body and attaches to empty dopamine receptors. In the brains of children or adults with ADHD, raclopride binding is higher, which indicates that these people have unusually low dopamine activity levels. An hour after stimulant ADHD medications are taken, raclopride binding is shown to fall to normal levels. This leads neuroscientists to propose that stimulants normalise dopamine function in the brains of people who are affected by ADHD.

Functional imaging provides researchers with information about activity in specific areas of subjects’ brains, before and during task performance. Functional magnetic resonance imaging (fMRI) shows oxygen uptake in areas of high nerve activity, and magnetoencephalography (MEG) reveals nerve activity in detail. A promising variant of fMRI, called fMRI-DTI (ie. diffusion tensor imaging), measures the connection between different regions of the brain. The ability of different regions of the brain to communicate with each other, known as crosstalk in neuroscientific parlance, is vital to brain function – in ADHD brains, crosstalk is significantly reduced.

Whilst only some types of imaging provide valid or generalisable information, a range of different techniques is used in brain imaging, and the reliable techniques provide useful insights into the brain’s wiring and structure. In order to better understand ADHD and to treat it more effectively, it is essential to know the wiring of the brain and how it operates.

Neuroimaging has shown that, in a child with ADHD, the brain is structurally different, whereby the ADHD child has a smaller prefrontal cortex and basal ganglia, and decreased volume of the posterior inferior vermis of the cerebellum, which all perform important functions in focussing and attending.

So, rather than being a difference in behavioural preference, it seems that ADHD can be partially attributed to a difference in how the brain is structured. What may look to the casual observer to behavioural choices, such as laziness, carelessness, and forgetfulness, are likely to be due to differences in the structure of the brain.

Researchers in England and Finland tracked forty-nine adolescents, who had been diagnosed with ADHD at age sixteen, and examined their brain structures and memory functions in young adulthood (between twenty and twenty-four years old), and compared them with a control group of thirty-four young adults. Their findings demonstrated that the group, which was diagnosed with ADHD in adolescence, had reduced brain volume in adulthood, leading to poorer memory function, even if they no longer met the diagnostic criteria for ADHD. Researchers observed that these subjects had less than normal volumes of grey matter in a region deep within the brain, the caudate nucleus, which integrates information from across different parts of the brain and supports cognitive functioning, including memory.

Because these structural differences persist into adulthood, for most children with ADHD, the probability that they will eventually grow out it is not as great as what was once thought. As many as three out of four adults, who had ADHD in childhood, continue to meet the ADHD diagnostic criteria in adulthood. Most of those, who actually do “outgrow” ADHD, continue to display many of the typical ADHD symptoms. Adults may score just below the cut-off on diagnostic checklists, but they are likely to continue to have abnormal brain structure, as well as functional impairments, both in their relationships and in their workplaces.

It was once proposed that each human function was assigned to a specific part of the brain, and that a part, which had been damaged by trauma or disease, permanently lost its function. Recent research has shown that the human brain is able to change in response to stimulation, a process known as neuroplasticity, which enables the brain to retain the ability to change from birth right through to old age. ADHD brains with deficits in one area are able to attempt to rewire themselves to accomplish a task.

Activities that can increase the brain’s effectiveness, such as meditation and mindfulness, can make significant changes in the brain. Working with people, who had never meditated before, researchers put one group through an eight-week mindfulness-based stress-reduction program and then compared them with a control group. The big difference they observed was in the posterior cingulate cortex, which is involved in mind wandering and self-awareness. Another observable change occurred in the left hippocampus, which helps with learning, cognition, memory, and emotional regulation. Later studies, which applied this research to ADHD participants, noted similar changes, in the ADHD group.

At Harvard University, researchers have been studying ADHD and non-ADHD subjects as they responded to a difficult cognitive task. While both groups were challenged by the task, the ADHD group subjects did not activate their anterior cingulate cortex, which plays two significant roles in attentional processing: adjusting the focus of one’s attention (where and when) as well as balancing the focus of attention (how much attention for how long). When tackling the task, the ADHD participants engaged a different, less specialised part of their brain.

This research emphasises what individuals with ADHD know only too well: it is really hard to figure out what to do and when to do it. This seems most likely to be due to their lack of ability to engage the most effective part of their brain, the anterior cingulate cortex.

The regions of the brain, which are active when no specific task is being performed are called the default mode network (DMN), which is involved in such mental exercises as daydreaming, an activity that has long been dismissed, both by researchers and by society at large. In the past, this was called the “resting state. However, since functional scans have shown how active the brain is at rest, the name has changed.

The DMN, which deals with task-irrelevant mental processes, mind-wandering, contemplation, and reflection, is comprised of the precuneus/posterior cingulate cortex, the medial prefrontal cortex, and the lateral and inferior parietal cortex. When individuals are at wakeful rest, engaged in internalised tasks, such as daydreaming, cogitating, ruminating, reminiscing, and pondering, the DMN is at its most active. Conversely, when individuals work on active, deliberate, goal-directed tasks, the DMN deactivates, and attentional pathways engage. In order to accommodate attentional demands, in people who do not have ADHD, the DMN and cognitive control networks work like a single pole changeover electrical switch – when one is turned on, the other automatically turns off, and they can be neither on nor off simultaneously.

In the ADHD person, when the attention circuits are activated, the daydreaming brain does not quieten down. Several studies, which have focussed on the connectivity of the DMN in individuals with ADHD, have shown that weak connections between control centres and the DMN cause an inability to modulate activity in the DMN. Many studies of children, adolescents, and adults with ADHD, both taking and not taking medication, have found that the balance between the cognitive control network and the DMN is either reduced, or absent, in those with the condition.

The lack of separation between the cognitive control network and the DMN in the ADHD brain provides a clue as to why the attention lapses. People with ADHD are capable of instructing their focus control system to pay attention to the task at hand, but the circuits that connect to the DMN do not send any instructions for it to quieten down. When the DMN notices something other than the task at hand, emotional interest centres light up and drown out the weak messages from the cognitive centres.

Whilst a lot has been learned since ADHD was seen simply as hyperactivity, before it was understood as a dysfunction in the control pathways, a lot remains to be investigated. Identifying those therapies which strengthen control centres, those therapies which improve communication between control centres and action centres, and those therapies which by-pass typical pathways, will help to enable people with ADHD to become more productive and confident.

The big thing in all of this for early childhood educators is for them to appreciate that the child with ADHD is not behaving wilfully, when he or she seems to be overly inattentive, easily distracted, fidgety or impulsive. In fact, the child is distracted by what is going on inside their brain, something that they cannot control and something that they simply cannot ignore. The idea that the child with ADHD has a disruptive behaviour disorder tends to suggest, at least to some people, that the child with ADHD is choosing to be deliberately “naughty” – the truth is that this child is struggling to resist the distractions produced by the way their brain is wired The last thing needed is for them to get into “trouble”.

Source: http://www.additudemag.com/adhd/article/12314.html