J Anesth Perioper Med. 2014;1(2):118-121. https://doi.org/10.24015/ebcmed.japm.2014.0017
From Department of Anesthesiology & Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA.
Correspondence to Dr. Roderic G. Eckenhoff at Roderic.Eckenhoff@uphs.upenn.edu.
EBCMED ID: ebcmed.japm.2014.0017 DOI: 10.24015/ebcmed.japm.2014.0017
In this short commentary, we attempt to convey the message that inflammation is well- positioned to be a major contributor of CNS pathology that may lead to the various forms of POCD. The combined influence of preexisting pathology and a second hit from surgery and inflammation could very well provoke an unrestrained sequence of events that are responsible for the cognitive pathology documented over the last few decades. Critical questions that remain unsolved are the role of anesthesia (anesthetics), whether resolution mechanisms are intact, and whether anti-inflammatory or pro-resolving strategies can be designed to mitigate POCD. Hampering progress has been the lumping of all cognitive disturbances as "POCD". It is certainly possible that delirium and acutely reversible POCD have different underlying mechanisms and pathologies compared to dementia or AD. Biomarker studies in human would help to provide a mechanism- based approach to diagnosis, terminology and ultimate treatment of POCD.
Declaration of Interests
No potential conflict of interest relevant to this opinion was reported.
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