Fragmented Sleep Enhances Postoperative Neuroinflammation but Not Cognitive Dysfunction: Really?
First, they showed there was a significant increase in hippocampal mRNA expression of interleukin-6 (IL-6) and tumor necrosis factor-α, but memory impairment was not further exacerbated when performing SF either preoperatively or postoperatively. Yang et al2 found that inflammatory pain may induce cognitive impairment through an IL-6-dependent mechanism. Wright et al3 performed a cross-sectional analysis of inflammatory marker levels and cognition in the stroke-free population-based cohort of the Northern Manhattan Study and found IL-6 levels were negatively associated with performance on the Mini-Mental State Examination. Thus, increasing mRNA expression of IL-6 should have been proportional to postoperative cognitive impairment.
Second, the authors suggest that the dissociation between neuroinflammation and cognitive decline may be related to their use of memory paradigms that do not capture all aspects of cognition or to a preconditioning effect. Because one test does not fit all changes in cognition, we suggest adding the Morris water maze test, the touchscreen test, or other tests to assess cognition of mice for preventing the interference of memory paradigm.4 Preconditioning reduces the expression of inflammatory cytokines. Lucchinetti et al5 found late preconditioning after sevoflurane inhalation decreased the expression of the proinflammatory L-selectin. Sun et al6 found hyperbaric oxygen preconditioning reduced systemic and hippocampal proinflammatory cytokines and mitigated surgery-induced cognitive impairment. Thus, we do not agree with the authors’ speculation.
In summary, it is too early for Vacas et al1 to conclude without additional experiments that perioperative SF significantly increases hippocampal inflammation with no additional cognitive impairment.