2014, Number 1
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Rev cubana med 2014; 53 (1)
Biochemical and molecular response to acute brain damage
Soler MCD, León PD, Larrondo MH, Godoy DA
Language: Spanish
References: 58
Page: 76-90
PDF size: 230.72 Kb.
ABSTRACT
Acute brain injury triggers, among others responses, a group of biochemical and
molecular disturbances that so far, are not enough characterized. These
disturbances enhance the previous brain damage or generate additional ischemic
insults amplifying this response. Dysglycemia, sodium and osmolarity disturbances,
and local and systemic inflammatory response are among the most relevant. As
their clinical pictures are different, and occasionally unnoticed, these disorders can
represent a real challenge for the intensivist. Biochemical and molecular
disturbances after an acute brain damage are not the priority in the management of
these patients, however it is important their early recognition, monitoring and
adequate treatment to avoid the secondary brain damage. Together with
hypoxemia and hypotension they can contribute significantly to worsen the
prognosis and mortality because they can define the magnitude of the final
neurologic deficit.
REFERENCES
Guyton A, Hall JE. Textbook of Medical Physiology. Cap. 61. Cerebral Blood Flow, Cerebrospinal Fluid, and BrainMetabolism. 11a ed. Philadelphia: Elsevier; 2006. pp. 761-8.
Losser MR, Damoisel C, Payen D. Glucose and stress conditions in the intensive care unit. Critical Care. 2010;14:231.
Chih CP, Lipton P, Roberts EL. Do active cerebral neurons really use lactate rather than glucose? Trends Neurosci. 2001;24:573-8.
Adams HP, Del Zoppo G, Alberts MJ. Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association. Stroke. 2007;38:1655-711.
Leng L, Metz CN, Fang Y, Xu J, Donnelly S, Baugh J, et al. MIF signal transduction initiated by binding to CD74. J Exp Med. 2003;197:1467-76.
Mizock BA. Alterations in fuel metabolism in critical illness: hyperglycaemia. Best Pract Res Clin Endocrinol Metab. 2001,15:533-551.
Halliwelli B, Gutteridge JMC. Free radicals in biology and medicine. Oxford: Clarendon Press; 1989. p. 142.
Leverve X. Hyperglycemia and oxidative stress: complex relationships with attractive prospects. Intensive Care Med. 2003;29:511-4.
Suh SW, Gum ET, Hamby AM, Chan PH, Swanson RA. Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase. J Clin Invest. 2007;117:910-8.
Dhindsa S, Tripathy D, Mohanty P, Ghanim H, Syed T, Aljada A, et al. Differential effects of glucose and alcohol on reactive oxygen species generation and intranuclear nuclear factor-kappa B in mononuclear cells. Metabolism. 2004;53:330-4.
Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation. 2002;106:2067-72.
Mazighi M, Labreuche J, Amarenco P. Glucose level and brain infarction: a prospective case-control study and prospective study. J Stroke. 2009 Oct; 4(5):346-51.
Allport LE,Baird TA, Davis SM. Hyperglycaemia and the ischaemic brain: continuous glucose monitoring and implications for therapy. Curr Diabetes Rev. 2008 Aug; 4(3):245-57.
Hermanides J, Vriesendorp TM, Bosman RJ, Zandstra DF, Hoekstra JB, Devries JH. Glucose variability is associated with intensive care unit mortality. Crit Care Med. 2010;38:838-42.
Helbo R, Schmidt JM, Kurtz P, Hanafy KA, Fernández L, Stuart RM, et al. Systemic glucose and brain energy metabolism after subarachnoid hemorrhage. Neurocrit Care. 2010;12:317-23.
Latorre JG, Chou SH, Nogueira RG, Singhal AB, Carter BS, Ogilvy CS, et al. Effective glycemic control with aggressive hyperglycemia management is associated with improved outcome in aneurysmal subarachnoid hemorrhage. Stroke. 2009;40:1644-52.
Naidech AM, Levasseur K, Liebling S. Moderate hypoglycemia is associated with vasospasm, cerebral infarction, and 3-month disability after subarachnoid hemorrhage. Neurocrit Care. 2010;12:181-7.
Piek J, Chesnut RM, Marshall LF, anBerkum-Clark M, Klauber MR, Blunt BA, et al. Extracranial complications of severe head injury. J Neurosurg.1992;77:901-7.
Schneider HJ, Kreitschmann-Andermahar I, Ghigo E, Stalla GK, Agha A. Hypothalamopituitary dysfunction following traumatic brain injury and aneurismal subarachnoid hemorrhage. JAMA. 2007;298:1429-38.
Agha A, Sherlock M, Phillips J, Tormey W, Thompson CJ. The natural history of post-traumatic neurohypophysal dysfunction. Eur J Endocrinol. 2005;152:371-7.
Tomlinson JW, Holden N, Hills RK. West Midlands Prospective Hypopituitary Study Group.Association between premature mortality and hypopituitarism. Lancet. 2001;357(9254):425-31.
Schneider HJ, Aimaretti G, Kreitschmann-Andermahr I, Stalla G, Ghigo E. Hypopituitarism. Lancet. 2007;369(9571):1461-70.
Moro N, Katayama Y, Igarashi T, Mori T, Kawamata T, Kojima J. Hyponatremia in patients with traumatic brain injury: incidence, mechanism, and response to sodium supplementation o retention therapy with hydrocortisone. Surg Neurol. 2007;68(4):387-93.
Sherlock M, O'Sullivan E, Agha A. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J. 2009;85(1002):171-5.
Tisdall M, Crocker M, Watkiss J, Smith M. Disturbances of Sodium in Critically Ill Adult Neurologic Patients. A Clinical Review. J Neurosurg Anesthesiol. 2006;18:57-63.
Cohan P, Wang C, McArthur DL. Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med. 2005;33(10):2358-66.
Verbalis JG. Inappropriate antidiuresis and other hypoosmolar states. En: Becker KL, editor. Principles and Practice of Endocrinology and Metabolism. 3 ed. Cap. 27. Philadelphia: Lippincott, Williams & Wilkins; 2001. Pp. 293-305.
Treggiari MM, Schutz N, Yanez ND, Romand JA. Role of intracranial pressure values and patterns in predicting outcome in traumatic brain injury: a systematic review. Neurocrit Care. 2007;6(2):104-12.
Dhar R, Murphy-Human T. A Bolus of Conivaptan Lowers Intracranial Pressure in a Patient with Hyponatremia after Traumatic Brain Injury. Neurocrit Care. 2011;14:97-102.
Sterns RH, Silver SM. Brain volume regulation in response to hypoosmolality and its correction. Am J Med. 2006;119(7 Suppl 1): S12-6.
Carpenter J, Weinstein S, Myseros J, Vezina G, Bell MJ. Inadvertent hyponatremia leading to acute cerebral edema and early evidence of herniation. Neurocrit Care. 2007;6:195-9.
Fraser CL, Arieff AI. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy. Am J Med. 1997;102(1):67-77.
Kumar S, Fowler M, Gonzalez-Toledo E, Jaffe SL. Central pontine myelinolysis, an update. Neurol Res. 2006;28(3):360-6.
Maggiore U, Picetti E, Antonucci E, Parenti E, RegolistiG, Mergoni M, et al. The relation between the incidence of hypernatremia and mortality in patients with severe traumatic brain injury. Critical Care. 2009;13:R110 (doi:10.1186/cc7953)
Black RM. Disorders of plasma sodium and plasma potassium. In: Irwin RS, Rippe JM, editors. Intensive Care Medicine. 5ta ed. Philadelphia: Lippincott Williams and Wilkins; 2003. p. 864-88.
Agha A, Thornton E, O'Kelly P, Tormey W, Phillips J, Thompson CJ. Posterior pituitary dysfunction after traumatic brain injury. J Clin Endocrinol Metab. 2004;89:5987-92.
Yaun X-Q, Wade CE. Neuroendocrine abnormalities in patients with traumatic brain injury. Frontiers in Neuroendocrinology. 1991;12:209-30.
Petit L, Masson F, Cottenceau V, Sztark F. Hypernatrémie contrôlée. Annales Françaises d' Anesthésie et de Réanimation. 2006:25:828-37.
Pierrakos C, Vincent JL. Sepsis biomarkers: a review. Critica lCare [revista en la Internet]. 2010 Ene [citado 4 nov 2011];14(R15): [aprox18p.]. Disponible en: http://ccforum.com/content/14/1/R15
American College of Chest Physicians/Society of Critical Care Medicine. American College of Chest Physicians/Society of Critical Care Medicine consensus conference; definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992;20(6):864-74.
Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS international sepsis definitions conference. Crit Care Med. 2003;31:1250-6.
Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal S, et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit Care Medicine. [revista en la Internet]. 2013 Feb [citado 24 abr 2013];41(2):[aprox 58 p.]. Disponible en: http:// www.ccmjournal.org
Perry VH. A revised view of the central nervous system microenvironment and major histocompatibility complex class II antigen presentation. J Neuroimmunol. 1998; 90:113-21.
Rojas J, González S,Patrucco L, Cristiano E. Rol de las Celulas T reguladoras en la Esclerosis Múltiple. Medicina (Buenos Aires). 2010; 70: 79-86 45. Cassan C, Liblau RS. Immune tolerance and control of CNS autoimmunity: from animal models to MS patients. J Neurochem. 2007;100:883-92.
Romano M. Mecanismos inflamatorios involucrados en el daño cerebral isquémico agudo. Posibles blancos terapéuticos. Factores pronósticos. Neurol Arg. 2011;3(03):176-81.
Aloisi F. Immune function of microglia. Glia. 2001;36:165-79.
Cuenca-López MD, Brea D, Segura T, Galindo MF, Anton-Martinez D, Águila J, et-al. La inflamación como agente terapeútico en el infarto cerebral: respuesta inflamatoria celular y mediadores inflamatorios. Rev Neurol. 2010; 0:349-59.
Garau A, Bertini R, Colotta F, Casilli F, Bigini P, Cagnotto A, et-al. Neuroprotection with the CXCl8 inhibitor repertaxin in transient brain ischemia. Cytokine. 2005;30:125-31.
Smith WL, Marnett LJ. Prostaglandin endoperoxide synthase: structure and catalysis. Biochim Biophys Acta. 1991;1083:1-17.
Lampl Y, Boaz M, Gilad R, Lorberboym M, Dabby R, Rapoport A, et-al. Minocycline treatment in acute stroke: an open label, evaluator-blinded study. Neurology. 2007;69:1404-10.
Melero-Fernández de Mera RM, García-Martínez E, Fernandez-Gomez FJ, Hernández-Guijo JM, Aguirre N, Galindo MF, et-al. ¿Es la vieja minociclina un nuevo fármaco neuroprotector? Rev Neurol. 2008;47:31-8.
Ducruet AF, Zacharia BE, Hickman ZL, Grobelny BT, Yeh ML, Sosunov SA, et-al. The complement cascade as a therapeutic target in intracerebral hemorrhage. Exp Neurol. 2009;219:398-403.
Burkhart CS, Siegemund M, Steiner LA. Cerebral perfusion in sepsis. Crit Care [revista en la Internet]. 2010 Feb [citado 04 nov 2011];14(215):[aprox 5p.]. Disponible en: http://ccforum.com/content/14/2/215
Booke M, Westphal M, Hinder F, Traber LD, Traber DL. Cerebral blood flow is not altered in sheep with Pseudomonas aeruginosa sepsis treated with norepinephrine or nitric oxide synthase inhibition. Anesth Analg. 2003,96:1122-8.
Sharshar T, Polito A, Checinski A, Stevens RD. Septic-associated encephalopathy - everything starts at a microlevel. Critical Care[revista en la Internet].2010 May [citado 4 nov 2011];14(199):[aprox 2p.].Disponible en: http://ccforum.com/content/14/5/199
Pfister D, Schmidt B, Smielewski P, et al.: Intracranial pressure in patients with sepsis. Acta Neurochir. Suppl 2008;102:71-5.
Oddo M, Carrera E, Claassen J, Mayer SA, Hirsch LJ. Continuous electroencephalography in the medical intensive care unit. Crit CareMed. 2009,37:2051-6.
Taccone FS, Su F, Pierrakos C, He X, James S, Dewitte O, et al. Cerebral microcirculation is impaired during sepsis: an experimental study. Critical Care[revista en la Internet]. 2010 Abril [4 nov 2011]; 14(140): [aprox 10p.]. Disponible en: http://ccforum.com/content/14/4/R140