Cingulate, frontal, and parietal cortical dysfunction in attention-deficit/hyperactivity disorder

Abstract

Functional and structural neuroimaging have identified abnormalities of the brain that are likely to contribute to the neuropathophysiology of attention-deficit/hyperactivity disorder (ADHD). In particular, hypofunction of the brain regions comprising the cingulo-frontal-parietal cognitive-attention network have been consistently observed across studies. These are major components of neural systems that are relevant to ADHD, including cognitive/attention networks, motor systems, and reward/feedback-based processing systems. Moreover, these areas interact with other brain circuits that have been implicated in ADHD, such as the "default mode" resting state network. The ADHD imaging data related to cingulo-frontal-parietal network dysfunction will be selectively highlighted here to help facilitate its integration with the other information presented in this special issue. Together, these reviews will help shed light on the neurobiology of ADHD.

Figure 1. The Cingulo-Frontal-Parietal Cognitive/Attention Network

The dorsal anterior midcingulate cortex [daMCC], dorsolateral prefrontal cortex [DLPFC], ventrolateral prefrontal cortex [VLPFC] and parietal cortex comprise the CFP network. These regions work in concert with each other and other regions such as striatum and cerebellum to support normal cognition, attention and motor control processes. All of these brain regions have been found to display functional and structural abnormalities in ADHD.

Figure 2. The daMCC Shows Hypofunction in ADHD during Counting Stroop

Dorsal anterior midcingulate cortex (daMCC) activated in healthy controls, but not in subjects with ADHD, during the Counting Stroop (30).

Figure 3. The daMCC Shows Hypofunction in ADHD during Response Inhibition

Tamm and colleagues (31) showed that daMCC was hypoactive in an ADHD group relative to control group during a response inhibition Go/NoGo task.

Figure 4. Meta-Analysis Shows daMCC and CFP Dysfunction in ADHD

Dickstein and colleagues (40), via an activation likelihood meta-analysis, found daMCC to be among a limited number of brain regions that were hypoactive in ADHD relative to healthy controls. CFP network abnormalities were also reported.

Figure 5. Methylphenidate increases daMCC and CFP activity in ADHD

Using the MSIT and fMRI in 21 adults with ADHD, Bush and colleagues (24) showed that at 6 weeks, daMCC activation was higher in the group that received methylphenidate (N = 11) than in the group that received placebo (N = 10). Similar results were observed in dorsolateral prefrontal cortex (DLPFC), parietal cortex and networked regions.