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Published on: March 19, 2018
Cerebrospinal Fluid Biomarker for Alzheimer Disease Predicts Postoperative Cognitive Dysfunction
Lisbeth Evered1, Brendan Silbert, David A Scott
1From the Centre for Anaesthesia and Cognitive Function, Department of Anaesthesia and Acute Pain Medicine, St. Vincent's Hospital, and Anaesthesia, Perioperative, and Pain Medicine Unit, Melbourne Medical School, University of Melbourne, Melbourne, Victoria, Australia (L.E., B.S., D.A.S.); Academic Unit for Psychiatry of Old Age, Department of Psychiatry, University of Melbourne, and National Ageing Research Institute, Parkville, Victoria, Australia (D.A.); Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia (P.M.); and Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Gothenburg, Sweden (K.B.).
Background:
Postoperative cognitive dysfunction (POCD) affects 16 to 21% of the elderly 3 months after anesthesia and surgery and is associated with adverse outcomes. The exact cause of POCD remains unknown. The authors hypothesized that elderly individuals with Alzheimer disease (AD) neuropathology, identified by cerebrospinal fluid (CSF) analysis, would have increased the risk for POCD.
Methods:
CSF samples were collected from 59 patients 60 yr or older who received combined spinal and general anesthesia for elective total hip replacement. Patients underwent neuropsychological testing preoperatively and at 7 days, 3 months, and 12 months postoperatively. POCD at 3 months and cognitive decline at 12 months were calculated by using the reliable change index. CSF amyloid β1-42 (Aβ1-42), total-tau, phosphorylated-tau, and neurofilament light were assayed with enzyme-linked immunosorbent assay methods.
Results:
POCD was identified in 5 of 57 patients (8.8%) at 3 months. For Aβ1-42, 11 patients were below the cut-point for AD neuropathology of whom 3 were classified with POCD (27.3%; 95% CI, 6.0 to 61%), whereas of the 46 patients above the cut-point, 2 were classified with POCD (4.3%; 95% CI, 0.5 to 14.8%) (P = 0.01). There was no significant difference in the incidence of POCD in relation to the cut-points for any of the other analytes.
Conclusions:
Low CSF Aβ1-42 may be a significant predictor of POCD at 3 months. This indicates that patients with AD neuropathology even in the absence of clinically detectable AD symptoms may be susceptible to POCD.
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