Changeux and collaborators look at the brain correlates of pathological gambling, evaluating whether addictions might occur because of a predisposition linked to abnormal functioning of a frontal circuitry associated with self awareness, preceding any use of drugs. Some clips:
The introduction of magnetoencephalography (MEG) has made it possible to study neural mechanisms even in deeper parts of the cortex with a high degree of temporal resolution in combination with a decent spatial resolution. This allows investigation of one of the major networks of the brain, the paralimbic interaction between the medial prefrontal/anterior cingulate (ACC) and medial parietal/posterior cingulate (PCC) cortices. This interaction has in several recent studies been associated with self-awareness.
Schematic representation of the medial cortical components of the paralimbic network of self-awareness. Schematic localization of the medial sources for MEG registration. Red, ACC; Blue, PCC.
They compared 14 pathological gamblers and 11 age- and sex-matched controls using a stop-signal task consisting of “go” and “nogo” trials. In go trials, the participant is instructed to press a button as soon as an “O” appears on the screen. In nogo trials, the O is followed by an “X,” and the participant is instructed to withhold his response. The task can be used to measure a number of variables associated with impulsivity such as the stop-signal reaction time (SSRT), which is the time required for the stop signal to be processed so a response can be withheld. In particular, the SSRT has been widely used as a valid measure of impulsivity in general, and in studies of patients suffering from addiction.
The main finding of the present study was that behavioral addiction is linked to abnormal activity in, and communication between, nodal regions of the paralimbic network of self-awareness, the ACC and PCC, which are effective in different aspects of self-awareness processing. Pathological gamblers had lower synchronization between the ACC and PCC at rest in the high gamma band compared with controls, and failed to show an increase in gamma synchronization during rest compared with the task (as observed in controls). These findings could not be attributed to previous drug abuse or smoking habits. Furthermore, pathological gamblers without previous drug abuse had lower PCC power than controls and gamblers with previous stimulant abuse during the stop-signal task. In contrast, a history of stimulant abuse in gamblers caused a marked increase in power across regions and frequencies both at rest and during the stop-signal task.
