Circulating Catecholamines and Sympathetic Activity after Head Injury
Abstract
Plasma norepinephrine (NE) and dopamine beta-hydroxylase (DBH) levels were measured during the first 7 days after head injury in 48 patients. Blood pressure, pulse, temperature, and Glasgow coma score (GCS) were recorded at the time of sampling for each patient, and the relationships of these to NE and DBH were examined. In patients with multiple trauma, NE levels were usually elevated, regardless of the GCS. In patients with head injury alone, however, NE was proportional to GCS. Alert patients after a brief loss of consciousness (GCS, 14) had normal NE levels. Those in coma had levels as high as 7 times normal. Blood pressure, pulse, and temperature were found to be elevated proportionally to elevations in plasma NE in patients with head injury. The finding of elevated plasma NE in patients with severe head injury raises the possibility of adverse effects of sympathetic hyperactivity in patients with severe head injury, including hypermetabolism, cardiovascular abnormalities, and direct effects of catecholamines on the damaged central nervous system.
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Second-impact syndrome is thought to result from abrupt post-traumatic loss of cerebral blood flow autoregulation and catecholamine release that create a rapid increase in intracranial blood volume and catastrophic cerebral edema.
“SIS is thought to result from abrupt post-traumatic loss of cerebral blood flow autoregulation and catecholamine release that create a rapid increase in intracranial blood volume and catastrophic cerebral edema [32, 105].”
From The neuropathology of sport (2014) · cites this paper as [32]
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McKee, A. C., & Daneshvar, D. H. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-52892-6.00004-0 · Cited by 829 · see citing works
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Rovlias, A., & Kotsou, S. (2000) · Neurosurgery · doi:10.1097/00006123-200002000-00015 · Cited by 419 · see citing works
McKee, A. C., Daneshvar, D. H., Alvarez, V. E., & Stein, T. D. (2014) · Acta Neuropathologica · doi:10.1007/s00401-013-1230-6 · Cited by 422 · see citing works
“Although the definition of SIS is controversial and some investigators have challenged its existence [123], SIS is thought to result from abrupt posttraumatic loss of cerebral blood flow autoregulation and catecholamine release that create a rapid increase in intracranial blood volume and catastrophic cerebral edema […”
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Lam, A. M., Winn, H. R., Cullen, B. F., & Sundling, N. (1991) · Journal of neurosurgery · doi:10.3171/jns.1991.75.4.0545 · Cited by 347 · see citing works
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Alam, A., Thelin, E. P., Tajsic, T., Khan, D. Z., Khellaf, A., Patani, R., & Helmy, A. E. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-02005-x · Cited by 298 · see citing works
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Moppett, I. K. (2007) · British Journal of Anaesthesia · doi:10.1093/bja/aem128 · Cited by 286 · see citing works
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Hibbard, M. R., Bogdany, J., Uysal, S., Kepler, K., Silver, J., Gordon, W. A., & Haddad, L. B. (2000) · Brain Injury · doi:10.1080/026990500120925 · Cited by 291 · see citing works
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Ott, L. G., McClain, C. J., Gillespie, M. N., & Young, B. A. (1994) · Journal of Neurotrauma · doi:10.1089/neu.1994.11.447 · Cited by 265 · see citing works
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BackgroundInfluentialBrain-gut axis dysfunction in the pathogenesis of traumatic brain injury
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Catecholamines predict outcome in traumatic brain injury
Hamill, R. W., Woolf, P. D., McDonald, J. V., Lee, L. A., & Kelly, M. M. (1987) · Annals of Neurology · doi:10.1002/ana.410210504 · Cited by 217 · see citing works
Dysautonomia after traumatic brain injury: a forgotten syndrome?
Baguley, I. J., Nicholls, J., Felmingham, K. L., Crooks, J., Gurka, J. A., & Wade, L. D. (1999) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.67.1.39 · Cited by 213 · see citing works
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Rosner, M. J., Newsome, H. H., & Becker, D. P. (1984) · Journal of neurosurgery · doi:10.3171/jns.1984.61.1.0076 · Cited by 209 · see citing works
Young, B. A., Ott, L. G., Dempsey, R. J., Haack, D. G., & Tibbs, P. A. (1989) · Annals of Surgery · doi:10.1097/00000658-198910000-00007 · Cited by 204 · see citing works
Battista, A. P. D., Rhind, S. G., Hutchison, M. G., et al. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0500-3 · Cited by 188 · see citing works
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The Effects of Traumatic Brain Injury on Regional Cerebral Blood Flow in Rats
Yuan, X. Q., Prough, D. S., Smith, T. L., & DeWitt, D. S. (1988) · Journal of Neurotrauma · doi:10.1089/neu.1988.5.289 · Cited by 181 · see citing works
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Ventricular fluid interleukin-1 activity in patients with head injury.
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Inao, S., Marmarou, A., Clarke, G. D., Andersen, B. J., Fatouros, P. P., & Young, H. F. (1988) · Journal of neurosurgery · doi:10.3171/jns.1988.69.5.0736 · Cited by 145 · see citing works
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ZARITSKY, A. L., & Chernow, B. (1984) · The Journal of Pediatrics · doi:10.1016/s0022-3476(84)80003-7 · Cited by 143 · see citing works
Post-traumatic neurodegeneration and chronic traumatic encephalopathy
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DeWitt, D. S., Prough, D. S., Taylor, C. L., & Whitley, J. M. (1992) · Journal of neurosurgery · doi:10.3171/jns.1992.76.5.0812 · Cited by 126 · see citing works
Systemic complications after head injury: a clinical review
Lim, H. B., & Smith, M. (2007) · Anaesthesia · doi:10.1111/j.1365-2044.2007.04998.x · Cited by 125 · see citing works
Catecholamines as outcome markers in isolated traumatic brain injury: the COMA-TBI study
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Sequelae following traumatic brain injury The cerebrovascular perspective
Golding, E. M. (2002) · Brain Research Reviews · doi:10.1016/s0165-0173(02)00141-8 · Cited by 115 · see citing works
Bruder, N. J., Raynal, M., Pellissier, D., Courtinat, C., & François, G. (1998) · Critical Care Medicine · doi:10.1097/00003246-199803000-00033 · Cited by 110 · see citing works
Černak, I., Savić, V., Kotur, J., Prokić, V., Veljović, M., & Grbovic, D. (2000) · Journal of Neurotrauma · doi:10.1089/neu.2000.17.53 · Cited by 111 · see citing works
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Lv, L., Hou, L., Yu, M., et al. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2010.1391 · Cited by 106 · see citing works
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Raymont, V., Greathouse, A. D., Reding, K. M., Lipsky, R. H., Salazar, A. Μ., & Grafman, J. H. (2007) · Brain · doi:10.1093/brain/awm300 · Cited by 102 · see citing works
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BackgroundVillalba, N., Sackheim, A. M., Nunez, I. A., Hill-Eubanks, D. C., Nelson, M. T., Wellman, G. C., & Freeman, K. (2017) · Journal of Neurotrauma · doi:10.1089/neu.2015.4340 · Cited by 99 · see citing works
Fern??ndez-Ortega, J. F., Prieto-Palomino, M. Á., pez, A. M. O.-L., et al. (2006) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/01.ta.0000197634.83217.80 · Cited by 99 · see citing works
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Choi, H. A., Jeon, S., Samuel, S., Allison, T. A., & Lee, K. (2013) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-013-0370-3 · Cited by 95 · see citing works
Intracranial mechanisms for preserving brain blood flow in health and disease
McBryde, F. D., Malpas, S. C., & Paton, J. F. R. (2016) · Acta Physiologica · doi:10.1111/apha.12706 · Cited by 96 · see citing works
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“Adrenaline and noradrenaline blood levels increase following TBI; their circulatory levels can rise up to 500-fold and 100-fold, respectively [114], and remain elevated several days after injury [115].”
Beta‐Blocker Therapy in Severe Traumatic Brain Injury: A Prospective Randomized Controlled Trial
Khalili, H., Ahl, R., Paydar, S., Sjölin, G., Cao, Y., Fard, H. A., Niakan, A., Hanna, K., Joseph, B. A., & Mohseni, S. (2020) · World Journal of Surgery · doi:10.1007/s00268-020-05391-8 · Cited by 89 · see citing works
Gruenbaum, S. E., Zlotnik, A., Gruenbaum, B. F., Hersey, D., & Bilotta, F. (2016) · CNS Drugs · doi:10.1007/s40263-016-0355-2 · Cited by 86 · see citing works
“Severe TBI is often associated with a tremendous catecholamine surge, known as ‘paroxysmal sympathetic storm’, which may result in worsening secondary brain damage and multi-organ failure [29].”
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Singer, A. W., Jaax, N. K., Graham, J. S., et al. (1987) · Toxicology Letters · doi:10.1016/0378-4274(87)90192-5 · Cited by 86 · see citing works
Shohami, E., Gati, I., Beit‐Yannai, E., Trembovler, V., & Kohen, R. (1999) · Journal of Neurotrauma · doi:10.1089/neu.1999.16.365 · Cited by 85 · see citing works
“Acute insults to the central nervous system trigger a cascade of events involving an immediate and short-lived "explosion" of sympathetic discharge, with a massive rise in circulating catecholamines (Clifton et al., 1981; Ros-ner et al., 1984).”
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“84 Head AIS 5 308 138 135 (44) 29 (21) 0.”
Hyperglycemia in dogs and cats with head trauma: 122 cases (1997–1999)
Syring, R. S., Otto, C. M., & Drobatz, K. J. (2001) · Journal of the American Veterinary Medical Association · doi:10.2460/javma.2001.218.1124 · Cited by 84 · see citing works
Krakau, K., Omne-Pontén, M., Karlsson, T., & Borg, J. (2006) · Brain Injury · doi:10.1080/02699050500487571 · Cited by 85 · see citing works
The blood leukocyte count and its prognostic significance in severe head injury
Rovlias, A., & Kotsou, S. (2001) · Surgical Neurology · doi:10.1016/s0090-3019(01)00414-1 · Cited by 82 · see citing works
Physiological and metabolic response to isolated closed-head injury
Deutschman, C. S., Konstantinides, F. N., Raup, S., Thienprasit, P., & Cerra, F. B. (1986) · Journal of neurosurgery · doi:10.3171/jns.1986.64.1.0089 · Cited by 80 · see citing works
Kobori, N., Clifton, G. L., & Dash, P. K. (2006) · Journal of Neurotrauma · doi:10.1089/neu.2006.23.1094 · Cited by 80 · see citing works
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Self-citationThe Influence of Alcohol on Mortality in Traumatic Brain Injury
Opreanu, R. C., Kuhn, D., & Basson, M. (2010) · Journal of the American College of Surgeons · doi:10.1016/j.jamcollsurg.2010.01.036 · Cited by 75 · see citing works
Effects of Catecholamines on Oxygen Consumption and Oxygen Delivery in Critically III Patients
Chioléro, R. L., Flatt, J. P., Revelly, J., et al. (1991) · CHEST Journal · doi:10.1378/chest.100.6.1676 · Cited by 79 · see citing works
Chronic Pain-Associated Cardiovascular Disease: The Role of Sympathetic Nerve Activity
Reynolds, C. A., & Minić, Ž. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24065378 · Cited by 77 · see citing works
Purkayastha, S., Stokes, M. A., & Bell, K. R. (2019) · Brain Injury · doi:10.1080/02699052.2019.1631488 · Cited by 76 · see citing works
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BackgroundKrakau, K., Hansson, A., Karlsson, T., de Boussard, C. N., Tengvar, C., & Borg, J. (2007) · Nutrition · doi:10.1016/j.nut.2007.01.010 · Cited by 76 · see citing works
Skoglund, K., Enblad, P., Hillered, L., & Marklund, N. (2011) · Critical Care Medicine · doi:10.1097/ccm.0b013e31822d7dbd · Cited by 72 · see citing works
The Neglected Prehospital Phase of Head Injury: Apnea and Catecholamine Surge
Atkinson, J. L. D. (2000) · Mayo Clinic Proceedings · doi:10.4065/75.1.37 · Cited by 72 · see citing works
Walia, S. K., & Sutcliffe, A. J. (2002) · Injury · doi:10.1016/s0020-1383(02)00053-0 · Cited by 72 · see citing works
“In the head injured patient, plasma noradrenaline levels correlate with GCS score [20–22] and outcome [22–24].”
BackgroundAutonomic Nervous System Function in Patients with Acute Brainstem Stroke
Meglič, B., Kobal, J., Osredkar, J., & Pogačnik, T. (2001) · Cerebrovascular Diseases · doi:10.1159/000047605 · Cited by 70 · see citing works
“Such patients are not able to perform Valsalva or orthostatic manoeuvres, which are commonly performed for routine autonomic testing.Another method commonly used for evaluation of the ANS function in acute stroke patients is plasma catecholamines (norepinephrine and epinephrine) assay. Elevated plasma catecholamines a…”
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Stanislav, S. W. (1997) · Brain Injury · doi:10.1080/026990597123494 · Cited by 70 · see citing works
Nutrition and the neurosurgical patient
Gadisseux, P., Ward, J. D., Young, H. F., & Becker, D. P. (1984) · Journal of neurosurgery · doi:10.3171/jns.1984.60.2.0219 · Cited by 70 · see citing works
Time for a change to assess and evaluate body temperature in clinical practice
Sund‐Levander, M., & Grodzinsky, E. (2009) · International Journal of Nursing Practice · doi:10.1111/j.1440-172x.2009.01756.x · Cited by 67 · see citing works
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Ko, A., Harada, M. Y., Barmparas, G., Thomsen, G. M., Alban, R. F., Bloom, M. B., Chung, R., Melo, N., Margulies, D. R., & Ley, E. J. (2016) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0000000000000959 · Cited by 67 · see citing works
“Early propranolol administration may offset the elevation of catecholamines associated with sympathetic hyperactivity apparent in the first week after the injury.(24) In our current study, patients received a standard dose of 1 mg IV propranolol every 6 hours within 5.”
BackgroundWoolf, P. D., Hamill, R. W., McDonald, J. V., Lee, L. A., & Kelly, M. M. (1986) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1986.tb01691.x · Cited by 67 · see citing works
Multipotential and systemic effects of traumatic brain injury
Sabet, N., Soltani, Z., & Khaksari, M. (2021) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2021.577619 · Cited by 67 · see citing works
Traumatic brain injury and β-blockers
Schroeppel, T. J., Sharpe, J. P., Magnotti, L. J., et al. (2014) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0000000000000104 · Cited by 66 · see citing works
“This surge is on a gradient withmore severe TBIs resulting in higher levels of catecholamines.(6,7,9,30,31) Catecholamine excess often leads to extracranialmanifestations includingcardiacarrhythmia,noncardiogenic pulmonary edema, and immunosuppression.”
BackgroundBromocriptine for the management of autonomic dysfunction after severe traumatic brain injury
Russo, R., & O’Flaherty, S. (2000) · Journal of Paediatrics and Child Health · doi:10.1046/j.1440-1754.2000.00485.x · Cited by 65 · see citing works
Beta-Adrenergic Blockade and Traumatic Brain Injury: Protective?
Schroeppel, T. J., Fischer, P. E., Zarzaur, B. L., et al. (2010) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0b013e3181e981b8 · Cited by 64 · see citing works
Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury
Fernández-Ortega, J. F., Baguley, I. J., Gates, T. A., García-Caballero, M., Quesada-Garcia, J. G., & Prieto-Palomino, M. Á. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4364 · Cited by 64 · see citing works
The Metabolic Response to Acute Traumatic Brain Injury and Implications for Nutritional Support
Pepe, J. L., & Barba, C. A. (1999) · Journal of Head Trauma Rehabilitation · doi:10.1097/00001199-199910000-00007 · Cited by 63 · see citing works
Severe traumatic head injury in adults: Which patients are at risk of early hyperthermia?
Geffroy, A., Bronchard, R., Merckx, P., et al. (2004) · Intensive Care Medicine · doi:10.1007/s00134-004-2280-y · Cited by 61 · see citing works
“This sympathetic response is closely related to the severity of initial brain injury [ 22 ]; hence, releasing of neutrophils store by catecholamine could account for a major part in posttraumatic leukocytosis [21].”
BackgroundNeuroleptic malignant syndrome: A study of CSF monoamine metabolism
Nisijima, K., & Ishiguro, T. (1990) · Biological Psychiatry · doi:10.1016/0006-3223(90)90002-j · Cited by 61 · see citing works
Yang, S., Zhang, S., & Wang, M.-L. (1995) · Surgical Neurology · doi:10.1016/0090-3019(96)80243-6 · Cited by 61 · see citing works
Systemic arterial hypertension in head trauma
Simard, J. M., & Bellefleur, M. (1989) · The American Journal of Cardiology · doi:10.1016/0002-9149(89)90403-7 · Cited by 61 · see citing works
Hyponatremia and Brain Injury: Historical and Contemporary Perspectives
Kirkman, M. A., Albert, A. F., Ibrahim, A. G., et al. (2012) · Neurocritical Care · doi:10.1007/s12028-012-9805-y · Cited by 59 · see citing works
“This could mimic the clinical presentation of CSW, more so if combined with significant adrenergenic hormone release (elevated in patients with major brain pathology) [73] or administration, including norepinephrine or dopamine, also a diuretic and natriuretic in its own right (Fig.”
BackgroundIsolated Brain Injury as a Cause of Hypotension in the Blunt Trauma Patient
Mahoney, E. J., Biffl, W. L., Harrington, D. T., & Cioffi, W. G. (2003) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/01.ta.0000100381.89107.93 · Cited by 56 · see citing works
Young, B. A., Ott, L. G., Yingling, B., & McClain, C. J. (1992) · Journal of Neurotrauma · doi:10.1177/089771519200901s36 · Cited by 58 · see citing works
“Counterregulatory hormones that increased after severe head injury include blood and urine catecholamines, blood glucagon, and blood cortisol (Chiolero et al., 1989; Clifton et al., 1981; Haider et al., 1975a; Hortnagl et a!., 1980).”
Jacome, T. H., & Tatum, D. M. (2017) · Neurocritical Care · doi:10.1007/s12028-017-0410-y · Cited by 56 · see citing works
Grände, P. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00315 · Cited by 56 · see citing works
“It is well established that head-injured patients develop an adverse hyperadrenergic state with increase in proinflammatory sympathetic discharge and catecholamine release (42, 59).”
BackgroundHepatic Drug Metabolism in Critical Illness
McKindley, D. S., Hanes, S. D., & Boucher, B. A. (1998) · Pharmacotherapy The Journal of Human Pharmacology and Drug Therapy · doi:10.1002/j.1875-9114.1998.tb03898.x · Cited by 53 · see citing works
β-Blocker Exposure in Patients With Severe Traumatic Brain Injury (TBI) and Cardiac Uncoupling
Riordan, W. P., Cotton, B. A., Norris, P. R., et al. (2007) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0b013e3181271c34 · Cited by 52 · see citing works
Raj, R., Mikkonen, E. D., Siironen, J. O., Hernesniemi, J. A., Lappalainen, J., & Skrifvars, M. B. (2015) · Journal of neurosurgery · doi:10.3171/2015.4.jns141746 · Cited by 50 · see citing works
Palmieri, M., Frati, A., Santoro, A., Frati, P., Fineschi, V., & Pesce, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910865 · Cited by 49 · see citing works
“Changes in glycemia levels in severe TBI are related to the increased blood levels of catecholamines caused by the sympathetic hyperactivity after the traumatic injury [19,20].”
BackgroundTraumatic brain injury stimulates hippocampal catechol-O-methyl transferase expression in microglia
Redell, J. B., & Dash, P. K. (2006) · Neuroscience Letters · doi:10.1016/j.neulet.2006.11.060 · Cited by 49 · see citing works
“In the present study, the selection of COMT for a more detailed analysis was guided by a number of previous studies that have implicated catecholamine signaling in the behavioral sequelae of TBI [4,20,21].”
BackgroundCatecholamine response to a gradual increase of intracranial pressure
van Loon, J., Shivalkar, B., Plets, C., et al. (1993) · Journal of neurosurgery · doi:10.3171/jns.1993.79.5.0705 · Cited by 48 · see citing works
Marklund, N. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00540 · Cited by 46 · see citing works
O’Meara, A. I., Sequeira, J., & Ferguson, N. M. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.00118 · Cited by 47 · see citing works
The Metabolic Response to Brain Injury
Ott, L. G., Young, B., & McClain, C. J. (1987) · Journal of Parenteral and Enteral Nutrition · doi:10.1177/0148607187011005488 · Cited by 46 · see citing works
The neuroendocrinology of physical injury
Barton, R. N. (1987) · Baillière s Clinical Endocrinology and Metabolism · doi:10.1016/s0950-351x(87)80067-8 · Cited by 46 · see citing works
Incidence, Risk Factors, and Outcomes for Atrial Arrhythmias in Trauma Patients
Hadjizacharia, P., O’Keeffe, T., Brown, C., et al. (2011) · The American Surgeon · doi:10.1177/000313481107700526 · Cited by 45 · see citing works
β-Blockers for traumatic brain injury: A systematic review and meta-analysis
Ding, H., Liao, L., Zheng, X., Wang, Q., Liu, Z., Xu, G., Li, X., & Liu, L. (2021) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0000000000003094 · Cited by 46 · see citing works
Severe traumatic brain injury management and clinical outcome using the Lund concept
Koskinen, L., Olivecrona, M., & Grände, P. O. (2014) · Neuroscience · doi:10.1016/j.neuroscience.2014.06.039 · Cited by 44 · see citing works
“Head-injured patients are severely stressed with a markedly raised concentration of catecholamines in plasma (Clifton et al., 1981).”
BackgroundCardiac Reactive Oxygen Species After Traumatic Brain Injury
Larson, B., Stockwell, D. W., Boas, S., Andrews, T. J., Wellman, G. C., Lockette, W. E., & Freeman, K. (2011) · Journal of Surgical Research · doi:10.1016/j.jss.2011.09.056 · Cited by 43 · see citing works
- Authors
- Clifton, G. L., Ziegler, M. G., & Grossman, R. G.
- Affiliations
- University of California San Diego (US)
- Venue
- Neurosurgery
- Published
- 1981-01
- Volume
- 8
- Issue
- 1
- Pages
- 10-14
- ISSN
- 0148-396X (ISSN-L)
- OpenAlex
- W1988160703
- Cited by
- 296
- References
- 0
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 8 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 8 · 2019: 6 · 2018: 6 · 2017: 20 · 2016: 16 · 2015: 14 · 2014: 8 · 2013: 2 · 2012: 6
- FWCI
- 4.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurosurgery (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Emergency Medicine › Trauma and Emergency Care Studies
- Keywords
- traumatic brain injury, norepinephrine, dopamine beta-hydroxylase, circulating catecholamines, sympathetic hyperactivity, Glasgow coma score, coma, polytrauma, blood pressure, pulses, body temperature, hypermetabolism, cardiovascular anomalies
- MeSH terms
- Blood Pressure, Brain Injuries, Catecholamines, Coma, Dopamine beta-Hydroxylase, Humans, Norepinephrine, Sympathetic Nervous System
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