critical illness; hippocampus; inflammation; neurodegenerative disorders; structural MRI; Adult; Aged; Atrophy/pathology; Brain Diseases/blood; Brain Diseases/pathology; Critical Illness; Female; Hippocampus/pathology; Humans; Magnetic Resonance Imaging; Male; Middle Aged; White Matter/pathology; Young Adult; Atrophy; Brain Diseases; White Matter; Neurology; Neurology (clinical)
Abstract :
[en] [en] BACKGROUND AND PURPOSE: Hippocampal atrophy is presumably one morphological sign of critical illness encephalopathy; however, predictors have not yet been determined.
METHODS: The data for this report derived from patients treated at the intensive care units (ICUs) of the University Hospital in Bonn in the years 2004-2006. These patients underwent structural magnetic resonance imaging 6-24 months after discharge. Volumes (intracranial, whole brain, white matter, grey matter, cerebral spinal fluid, bilateral hippocampus) were compared with healthy controls. Pro-inflammatory parameters and ICU scoring systems were explored in conjunction with brain volumes. Cut-scores were defined to differentiate patients with high from those with low inflammatory response.
RESULTS: Hippocampal and white matter volume were reduced in critically ill patients compared with healthy controls. Procalcitonin showed a very strong correlation (r = -0.903, P = 0.01) and interleukin-6 a moderate correlation (r = -0.538, P = 0.031) with hippocampal volume, but not with other brain volumes. C-reactive protein was linked to grey matter volume. There was no correlation with systemic inflammatory response syndrome criteria (body temperature, heart rate, respiratory rate, white blood cell count) or for hippocampal or whole brain volume. Furthermore, parameters representing severity of disease (APACHE II score, SOFA score, duration of stay and duration of mechanical ventilation) were not associated with hippocampal or other brain volumes.
CONCLUSIONS: This analysis suggests that high levels of procalcitonin and interleukin-6 in the blood serum of critically ill patients are associated with a high likelihood of hippocampal atrophy irrespective of the severity of disease measured by ICU scoring systems and other inflammatory parameters.
Disciplines :
Neurology
Author, co-author :
Lindlau, A; Clinical Neuroscience Unit, Department of Neurology, University Hospital Bonn, Bonn, Germany
Widmann, C N; Clinical Neuroscience Unit, Department of Neurology, University Hospital Bonn, Bonn, Germany ; German Centre for Neurodegenerative Diseases (DZNE), Bonn, Germany
Putensen, C; Surgical Intensive Care, Department of Anaesthesiology and Intensive Care Medicine, University Hospital Bonn, Bonn, Germany
Jessen, F; German Centre for Neurodegenerative Diseases (DZNE), Bonn, Germany ; Department of Psychiatry, University of Bonn, Bonn, Germany
Semmler, A; Clinical Neuroscience Unit, Department of Neurology, University Hospital Bonn, Bonn, Germany ; Department of Neurology, University Hospital Zurich, Zurich, Switzerland
HENEKA, Michael ; Clinical Neuroscience Unit, Department of Neurology, University Hospital Bonn, Bonn, Germany ; German Centre for Neurodegenerative Diseases (DZNE), Bonn, Germany
External co-authors :
yes
Language :
English
Title :
Predictors of hippocampal atrophy in critically ill patients.
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Bibliography
Stevens RD, Pronovost PJ. The spectrum of encephalopathy in critical illness. Semin Neurol 2006; 26: 440-451.
Pandharipande PP, Girard TD, Jackson JC, et al. Long-term cognitive impairment after critical illness. N Engl J Med 2013; 369: 1306-1316.
Semmler A, Widmann CN, Okulla T, Urbach H, Kaiser M, Widman G. Persistent cognitive impairment, hippocampal atrophy and EEG changes in sepsis survivors. J Neurol Neurosurg Psychiatry 2013; 84: 62-69.
Pustavoitau A, Stevens RD. Mechanisms of neurologic failure in critical illness. Crit Care Clin 2008; 24: 1-24.
Cunningham C. Microglia and neurodegeneration: the role of systemic inflammation. Glia 2012; 61: 71-90.
Perry VH. Contribution of systemic inflammation to chronic neurodegeneration. Acta Neuropathol 2010; 120: 277-286.
Suchyta MR, Jephson A, Hopkins RO. Neurologic changes during critical illness: brain imaging findings and neurobehavioral outcomes. Brain Imaging Behav 2010; 4: 22-34.
Hopkins RO, Jackson JC. Neuroimaging after critical illness: implications for neurorehabilitation outcome. NeuroRehabilitation 2012; 31: 311-318.
Bartsch T, ed. The Clinical Neurobiology of the Hippocampus. Oxford University Press: Oxford, 2012.
Woon FL, Sood S, Hedges DW. Hippocampal volume deficits associated with exposure to psychological trauma and posttraumatic stress disorder in adults: a meta-analysis. Prog Neuropsychopharmacol Biol Psychiatry 2010; 34: 1181-1188.
Fossati P, Radtchenko A, Boyer P. Neuroplasticity: from MRI to depressive symptoms. Eur Neuropsychopharmacol 2004; 14 (Suppl. 5): S503-S510.
Satizabal CL, Zhu YC, Mazoyer B, Dufouil C, Tzourio C. Circulating IL-6 and CRP are associated with MRI findings in the elderly: the 3C-Dijon Study. Neurology 2012; 78: 720-727.
Jefferson AL, Massaro JM, Wolf PA, et al. Inflammatory biomarkers are associated with total brain volume: the Framingham Heart Study. Neurology 2007; 68: 1032-1038.
Jessen F, Feyen L, Freymann K, et al. Volume reduction of the entorhinal cortex in subjective memory impairment. Neurobiol Aging 2006; 27: 1751-1756.
Tang BMP, Eslick GD, Craig JC, McLean AS. Accuracy of procalcitonin for sepsis diagnosis in critically ill patients: systematic review and meta-analysis. Lancet Infect Dis 2007; 7: 210-217.
Uzzan B, Cohen R, Nicolas P, Cucherat M, Perret G-Y. Procalcitonin as a diagnostic test for sepsis in critically ill adults and after surgery or trauma: a systematic review and meta-analysis. Crit Care Med 2006; 34: 1996-2003.
Lobo SMA, Lobo FRM, Bota DP, et al. C-reactive protein levels correlate with mortality and organ failure in critically ill patients. Chest 2003; 123: 2043-2049.
Weberpals M, Hermes M, Hermann S, et al. NOS2 gene deficiency protects from sepsis-induced long-term cognitive deficits. J Neurosci 2009; 29: 14177-14184.
Semmler A, Frisch C, Debeir T, et al. Long-term cognitive impairment, neuronal loss and reduced cortical cholinergic innervation after recovery from sepsis in a rodent model. Exp Neurol 2007; 204: 733-740.
Gunther ML, Morandi A, Krauskopf E, et al. The association between brain volumes, delirium duration, and cognitive outcomes in intensive care unit survivors: the VISIONS cohort magnetic resonance imaging study. Crit Care Med 2012; 40: 2022-2032.
Cerejeira J, Firmino H, Vaz-Serra A, Mukaetova-Ladinska EB. The neuroinflammatory hypothesis of delirium. Acta Neuropathol 2010; 119: 737-754.