Pathogenesis of septic encephalopathy

Current Opinion in Neurology

Volumn 22, Issue 3, 2009, Pages 283-287

  Pytel, Peter ^a   Alexander, Jessy J ^a  

^a UNIVERSITY OF CHICAGO   (United States)

Author keywords

Brain; Inflammation; Sepsis

Indexed keywords

GLIAL FIBRILLARY ACIDIC PROTEIN; INTERLEUKIN 6; MAGNESIUM; NEURON SPECIFIC ENOLASE; PROCALCITONIN; PROTEIN S100B; RILUZOLE;

BLOOD BRAIN BARRIER; BRAIN HYPOXIA; BRAIN INFECTION; BRAIN INJURY; BRAIN ISCHEMIA; CLINICAL FEATURE; DISEASE MARKER; ELECTROENCEPHALOGRAM; HUMAN; MICROCIRCULATION; NONHUMAN; PATHOGENESIS; PROPHYLAXIS; REVIEW; SEPTIC ENCEPHALOPATHY;

ANIMALS; BIOLOGICAL MARKERS; BLOOD-BRAIN BARRIER; CENTRAL NERVOUS SYSTEM BACTERIAL INFECTIONS; COMPLEMENT ACTIVATION; DISEASE MODELS, ANIMAL; HUMANS; HYPOXIA-ISCHEMIA, BRAIN; MICROCIRCULATION; SEPSIS;

EID: 67049171321     PISSN: 13507540     EISSN: None     Source Type: Journal    
DOI: 10.1097/WCO.0b013e32832b3101     Document Type: Review

References (61)

1. Ebersoldt M, Sharshar T, Annane D. Sepsis-associated delirium. Intensive Care Med 2007; 33:941-950. This study provides insights into the diagnosis of septic encephalopathy and shows that as brain can be one of the first organs affected, it need not be a secondary event in response to systemic aberrations.
2. Siami S, Annane D, Sharshar T. The encephalopathy in sepsis. Crit Care Clin 2008; 24:67-82.
3. Kunze K. Metabolic encephalopathies. J Neural 2002; 249:1150-1159.
4. Sprung CL, Peduzzi PN, Shatney CH, et al. Impact of encephalopathy on mortality in the sepsis syndrome. The Veterans Administration Systemic Sepsis Cooperative Study Group. Crit Care Med 1990; 18:801-806.
5. Eidelman LA, Putterman D, Putterman C, Sprung CL. The spectrum of septic encephalopathy. Definitions, etiologies, and mortalities. JAMA 1996; 275: 470-473.
6. Hopkins RO, Jackson JC. Long-term neurocognitive function after critical illness. Chest 2006; 130:869-878.
7. Hopkins RO, Jackson JC. Assessing neurocognitive outcomes after critical illness: are delirium and long-term cognitive impairments related? Curr Opin Crit Care 2006; 12:388-394.
8. Streck EL, Comim CM, Barichello T, Quevedo J. The septic brain. Neurochem Res 2008; 33:2171-2177.
9. Hopkins RO, Gale SD, Weaver LK. Brain atrophy and cognitive impairment in survivors of acute respiratory distress syndrome. Brain Inj 2006; 20:263-271.
10. 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 Neural 2007; 204:733-740.
11. Gunther ML, Jackson JC, Ely EW. Loss of IQ in the ICU brain injury without the nsult. Med Hypotheses 2007; 69:1179-1182. This work defines the relationship between long-term behavioral impairment, loss of connections between brain regions and the possible mechanisms through which it occurs.
12. Fioretto JR, Martin JG, Kurokawa CS, et al. lnterleukin-6 and procalcitonin in children with sepsis and septic shock. Cytokine 2008; 43:160-164.
13. Sharshar T, Annane D, de la Grandmaison GL, et al. The neuropathology of septic shock. Brain Pathol 2004; 14:21-33.
14. Sharshar T, Carlier R, Bernard F, et al. Brain lesions in septic shock: a magnetic resonance imaging study. Intensive Care Med 2007; 33:798-806.
15. Bartynski WS, Boardman JF, Zeigler ZR, et al. Posterior reversible encephalopathy syndrome in infection, sepsis, and shock. AJNR Am J Neuroradiol 2006; 27:2179-2190.
16. Bloomfield SM, McKinney J, Smith L, Brisman J. Reliability of S100B in predicting severity of central nervous system injury. Neurocrit Care 2007; 6:121-138.
17. Hsu AA, Fenton K, Weinstein S, et al. Neurological injury markers in children with septic shock. Pediatr Crit Care Med 2008; 9:245-251. Septic encephalopathy is a complex setting in which faster diagnosis leads to better recovery. This study shows the potential of S100B as an important candidate.
18. Pelinka LE, Kroepfl A, Schmidhammer R, et al. Glial fibrillary acidic protein in serum after traumatic brain injury and multiple trauma. J Trauma 2004; 57: 1006-1012.
19. Vissers JL, Mersch ME, Rosmalen CF, et al. Rapid immunoassay for the determination of glial fibrillary acidic protein (GFAP) in serum. Clin Chim Acta 2006; 366:336-340.
20. Nguyen DN, Spapen H, Su F, et al. Elevated serum levels of S-100beta protein and neuronspecific enolase are associated with brain injury in patients with severe sepsis and septic shock. Crit Care Med 2006; 34:1967-1974.
21. Piazza O, Russo E, Cotena S, et al. Elevated S100B levels do not correlate with the severity of encephalopathy during sepsis. Br J Anaesth 2007; 99:518-521.
22. Young GB, Bolton CF, Archibald YM, et al. The electroencephalogram in sepsis-associated encephalopathy. J Clin Neurophysiol 1992; 9:145-152.
23. Young GB, Bolton CF, Austin TW, et al. The encephalopathy associated with septic illness. Clin Invest Med 1990; 13:297-304.
24. Rosengarten B, Hecht M, Auch D, et al. Microcirculatory dysfunction in the brain precedes changes in evoked potentials in endotoxin-induced sepsis syndrome in rats. Cerebrovasc Dis 2007; 23:140-147.
25. Dubin A, Murias G, Sottile JP, et al. Effects of levosimendan and dobutamine in experimental acute endotoxemia: a preliminary controlled study. Intensive Care Med 2007; 33:485-494.
26. Levy RJ, Deutschman CS. Cytochrome c oxidase dysfunction in sepsis. Crit Care Med 2007; 35:S468-S475.
27. Kafa IM, Ari I, Kurt MA. The peri-microvascular edema in hippocampal CA1 area in a rat model of sepsis. Neuropathology 2007; 27:213-220.
28. Baumgart K, Simkova V, Wagner F, et al. Effect of SOD-1 over-expression on myocardial function during resuscitated murine septic shock. Intensive Care Med 2009; 35:344-349.
29. Barichello T, Machado RA, Constantino L, et al. Antioxidant treatment prevented late memory impairment in an animal model of sepsis. Crit Care Med 2007;35:2186-2190.
30. Nishioku T, Dohgu S, Takata F, et al. Detachment of brain pericytes from the basal lamina is involved in disruption of the blood-brain barrier caused by lipopolysaccharide-induced sepsis in mice. Cell Mol Neurobiol 2008 [Epub ahead of print].
31. Pan W, Yu C, Hsuchou H, et al. Neuroinflammation facilitates LIF entry into brain: role of TNF. Am J Physiol Cell Physio! 2008; 294:C1436-C1442.
32. Pan W, Hsuchou H, Yu C, Kastin AJ. Permeation of blood-bome IL15 across the blood-brain barrier and the effect of LPS. J Neurochem 2008; 106:313-319.
33. Hofer S, Bopp C, Hoerner C, et al. Injury of the blood brain barrier and upregulation of icam-1 in polymicrobial sepsis. J Surg Res 2008; 146:276-281.
34. Audoy-Remus J, Richard JF, Soulet D, et al. Rod-shaped monocytes patrol the brain vasculature and give rise to perivascular macrophages under the influence of proinflammatory cytokines and angiopoietin-2. J Neurosci 2008; 28:10187-10199.
35. Alexander JJ, Jacob A, Cunningham P, et al. TNF is a key mediator of septic encephalopathy acting through its receptor, TNF reoeptor-1. Neurochem Int 2008; 52:447-456.
36. Huang YH, Chang AY, Huang CM, et al. Proteomic analysis of lipopolysaccharide-induced apoptosis in PC12 cells. Proteomics 2002; 2:1220-1228.
37. Riedemann NC, Guo RF, Hollmann TJ, et al. Regulatory role of C5a in LPS-induced IL-6 production by neutrophils during sepsis. FASEB J 2004; 18:370-372.
38. Riedemann NC, Guo RF, Ward PA. The enigma of sepsis. J Clin Invest 2003; 112:460-467.
39. Nakae H, Endo S, Inada K, et al. Serum complement levels and severity of sepsis. Res Commun Chem Pathol Pharmacol 1994; 84:189-195.
40. Czermak BJ, Sarma V, Pierson CL, et al. Protective effects of C5a blockade in sepsis. Nat Med 1999; 5:788-792.
41. Huber-Lang M, Sarma VJ, Lu KT, et al. Role of C5a in multiorgan failure during sepsis. J Immunol 2001; 166:1193-1199.
42. Fischer MB, Prodeus AP, Nicholson-Weller A, et al. Increased susceptibility to endotoxin shock in complement C3- and C4-deficient mice is corrected by C1 inhibitor replacement. J Immunol 1997; 159:976-982.
43. Prodeus AP, Zhou X, Maurer M, et al. Impaired mast cell-dependent natural immunity in complement C3-deficient mice. Nature 1997; 390:172-175.
44. Jacob A, Hensley LK, Safratowich BD, et al. The role of the complement cascade in endotoxin-induced septic encephalopathy. Lab Invest 2007; 87:1186-1194. This study shows the key role of the complement cascade in septic encephalopathy and the potential therapeutic value.
45. Rittirsch D, Flierl MA, Ward PA. Harmful molecular mechanisms in sepsis. Nat Rev Immunol 2008; 8:776-787. This review gives the recent insights into molecular interactions and dysregulated immune response that occur during sepsis.
46. Rittirsch D, Flierl MA, Nadeau BA, et al. Functional roles for C5a receptors in sepsis. Nat Med 2008; 14:551-557.
47. Flierl MA, Rittirsch D, Chen AJ, et al. The complement anaphylatoxin C5a induces apoptosis in adrenomedullary cells during experimental sepsis. PLoS ONE 2008; 3:e2560.
48. Flierl MA, Rittirsch D, Nadeau BA, et al. Functions of the complement components C3 and C5 during sepsis. FASEB J 2008; 22:3483-3490.
49. Henry CJ, Huang Y, Wynne A, et al. Minocycline attenuates lipopolysacchar-ide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia. J Neuroinflammation 2008; 5:15.
50. Turkoglu OF, Eroglu H, Okutan O, et al. A comparative study of treatment for brain edema: magnesium sulphate versus dexamethasone sodium phosphate. J Clin Neurosci 2008; 15:60-65.
51. Rosengarten B, Walberer M, Allendoerfer J, et al. LPS-induced endotoxic shock does not cause early brain edema formation: an MRI study in rats. Inflamm Res 2008; 57:479-483.
52. Maeda S, Nakatsuka I, Hayashi Y, et al. Heme oxygenase-1 induction in the brain during lipopolysaccharide induced acute inflammation. Neuropsychiatr Dis Treat 2008; 4:663-667.
53. Handa O, Stephen J, Cepinskas G. Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsis. Am J Physiol Heart Circ Physiol 2008; 295:H1712-H1719.
54. Lopez A, Lorente JA, Steingrub J, et al. Multiplecenter, randomized, placebo-controlled, double-blind study of the nitric oxide synthase inhibitor 546C88: effect on survival in patients with septic shock. Crit Care Med 2004; 32:21-30.
55. Kadoi Y, Goto F. Selective inducible nitric oxide inhibition can restore hemodynamics, but does not improve neurological dysfunction in experimentally induced septic shock in rats. Anesth Analg 2004; 99:212-220.
56. Euser AG, Bullinger L, Cipolla MJ. Magnesium sulphate treatment decreases blood-brain barrier permeability during acute hypertension in pregnant rats. Exp Physiol 2008; 93:254-261.
57. Ghabriel MN, Thomas A, Vink R. Magnesium restores altered aquaporin-4 immunoreactivity following traumatic brain injury to a preinjury state. Acta Neurochir Suppl 2006; 96:402-406.
58. Esen F, Erdem T, Aktan D, et al. Effect of magnesium sulfate administration on blood-brain barrier in a rat model of intraperitoneal sepsis: a randomized controlled experimental study. Crit Care 2005; 9:R18-R23.
59. Toklu HZ, Uysal MK, Kabasakal L, et al. The effects of riluzole on neurological, brain biochemical and histological changes in early and late term of sepsis in rats. J Surg Res 2009; 152:238-248.
60. Umgelter A, Reindl W, Lutz J, et al. Treatment of septic patients with an arginine-based endotoxin adsorber column improves hemodynamics and reduces oxidative stress: results of a feasibility study. Blood Purif 2008; 26:333-339.
61. Wratten ML. Therapeutic approaches to reduce systemic inflammation in septic-associated neurologic complications. Eur J Anaesthesiol Suppl 2008; 42:1-7.