| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Anesthesia and Surgery, University of Manitoba, I.H. Asper Clinical Research Institute, CR3008-369 Tache Ave, Winnipeg, MB R2H 2A6, Canada
(Email: hgrocott{at}sbgh.mb.ca).
Adverse cognitive outcomes after cardiac surgery have been repeatedly described during the past several decades. Although much has been learned about the incidence, time course, pattern, and significance of this clinical entity, gaps remain in our understanding of its cause and pathophysiology. Studying the relationship between functional outcomes and their structural brain correlates using magnetic resonance imaging (MRI) is an important step in aiding understanding of cognitive outcomes after cardiac surgery. In doing so, Knipp and colleagues [1] have identified several important findings. The first replicates previous work demonstrating that early postoperative cognitive decline occurs after cardiac surgery and is often followed by a period of variable cognitive recovery. This recovery was found to be transient, with a recrudescence after several years. The initial loss, intermediate recovery, and then later deterioration are likely related to a phenomenon known as cognitive reserve; that is, if neuronal injury results in a loss of function, one’s brain can draw on functional reserves to make up for that loss in function. With the reserve capacity now having been depleted in the earlier postoperative period, the brain is more susceptible to "normal" age-related changes manifest as cognitive deficits.
A second important point relates to an evolving understanding pertaining to etiology. One of the speculative causes of early cognitive loss is overt cerebral ischemia with a loss of neurons. Although Knipp and colleagues’ MRI studies demonstrated some focal abnormalities in certain patients, there was no relationship to cognitive changes. There are several possible explanations for this lack of MRI-detectable ischemia. Either there was no ischemic injury (unlikely), or if the injury occurred, it was beneath the resolution of MRI. A more likely explanation is that the affected neurons may have been injured to the point of functional loss, but not that of necrosis. As good as conventional MRI is at defining lesions, functional MRI could conceivably have been much better at ascertaining a relationship to injury. Indeed, preliminary investigations have used functional MRI to detect changes in brain function after cardiac surgery.
Failing to find that functional losses are reflected by gross structural (anatomic) losses is not novel in itself, but the continued lack of a relationship over the multiyear follow-up period makes this study unique. A past explanation for the recrudescence of cognitive loss was thought to be related to ongoing ischemic losses patients experience due to their inherent vasculopathies. This study does not support this tenant. The search continues for a better understanding of the subtleties of brain injury after cardiac surgery.
 |
References |
|---|
 Top References |
|---|
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
