Cognitive function after open-heart surgery: Are postoperative neuropsychological deficits caused by cardiopulmonary bypass?

Despite the many technological developments in arterial perfusion and cardiac surgical procedures, open-heart surgery is still believed to pose a significant risk for cerebral injury. There are several potential causes of brain damage during open-heart surgery, including prolonged or severe arterial hypotension, as well as emboli emanating from the cardiopulmonary bypass circuit or the operative field. This article reviews the available neuropsychological studies of outcome following cardiac valve replacement and coronary artery bypass grafting. Because both procedures are life-saving operations, the research in this area has been quasi-experimental and fraught with methodological problems. Nonetheless, the findings converge to suggest that cognitive dysfunction occurs after open-heart surgery, and that the deficits are attributable, at least in part, to factors specific to the operation or to the patient being maintained on cardiopulmonary bypass. Preliminary findings suggest that embolization is the primary cause of perioperative deficits in uncomplicated operations. Studies have also consistently found preoperative deficits in this population, suggesting that neuropsychological dysfunction is caused by severe chronic cardiac disease as well as open-heart surgery.     

Visual slow brain potentials in children with attention deficit disorder

Using a two-stimulus reaction time paradigm, with two separate reward conditions (contingent and noncontingent), we compared slow wave brain potentials (ERPs) in 144 children with attention deficit disorder (ADD) and 30 normal control children. This article reviews the findings during the 900 msec visual warning stimulus. As we had expected, based on ERP work of Forth and Hare (1989) and Raine, Venables and Williams (1990), and on previous work from our own laboratory, the group differences were found in the negative slow wave portions of the ERP complex during the contingent reward condition but not during the noncontingent condition. Aggressive hyperactive subjects with attention deficit disorder (ADDHA) were discriminated from nonaggressive subjects (including control subjects) during the contingent reward condition in the following ways: (1) greater fronto-central negativity (640–900 msec slow wave) and (2) greater right parietal than left parietal negativity (430–750 msec slow wave). All ADD subgroups, when compared to control (CONTR) subjects, showed greater slow wave negativity (700–900 msec) at the midline occipital electrode site during the contingent reward condition. This could be explained in part as an IQ effect on ERPs reflecting the IQ difference between the ADD subgroups and the controls. These slow wave findings seem to relate to attentional problems of these children. They are discussed in terms of a psychobiological model of inhibition/disinhibition and appetitive activation.