A study of patients undergoing coronary artery bypass surgery finds evidence that these patients not only have cognitive deficits after the procedure, but that they may have memory deficits prior to surgery. The study, directed by researchers at the University of North Carolina at Wilmington, was published in the July issue of Neuropsychology and sparked a number of critical commentaries.
A possible common cause for both Alzheimer's disease and cardiovascular disease, perhaps related to cholesterol, has drawn interest in recent years. Among the research areas bordering this endeavor is the investigation into cognitive deficits found after coronary artery bypass surgery (CABG). There are clear signs of cognitive dysfunction immediately after surgery in as many as 75 percent of patients, and most of these problems are clearly a function of the abnormal physiological conditions of anesthesia and surgery, and they disappear within a week or two. A question that interests some researchers is whether there are more subtle, long-tem cognitive deficits in a subset of patients, and whether effects of CABG can be teased out from any subtle cognitive effects that were present before the surgery. A corollary to this latter question is whether any cognitive deficits seen before CABG in people with heart disease might in fact be preclinical Alzheimer's disease, rather than just a result of poor circulation to the brain.
The primary intention of the UNC-Wilmington study was to determine whether CABG produces cognitive deficits beyond the first few weeks after surgery. Study participants underwent psychological testing one to two days before CABG and then three to four weeks after surgery. The researchers report finding new postoperative impairments in attention in the study group, versus normal controls. In addition, they noted that even before surgery, the group destined for CABG had deficits on tests of memory. They point out that more research is needed to determine if the pretest deficits were caused by anxiety, poor circulation to the brain, dementia, or some combination of these.
The article is accompanied by four accompanying commentaries (and a response by the authors), some of which praise the ambitious scope of the paper, but all of which take the researchers to task for perceived flaws in study design or choice of statistical methodology. Several of the reviewers pose their critiques in the framework of a troublesome divide between academic neuropsychologists and clinicians. By one commentator's account, neuropsychologists should rely less on traditional parametric methods designed to answer questions about the underlying nature of disease, and should instead be generating conclusions that are useful to cardiologists who have to make treatment plans.—Hakon Heimer
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