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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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“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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The neuropathology of traumatic brain injury
McKee, A. C., & Daneshvar, D. H. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-52892-6.00004-0 · Cited by 899
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
“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 […”
BackgroundThe Influence of Hyperglycemia on Neurological Outcome in Patients with Severe Head Injury
Rovlias, A., & Kotsou, S. (2000) · Neurosurgery · doi:10.1097/00006123-200002000-00015 · Cited by 419
Hyperglycemia and neurological outcome in patients with head injury
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
Cellular infiltration in traumatic brain injury
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 309
Traumatic brain injury: assessment, resuscitation and early management
Moppett, I. K. (2007) · British Journal of Anaesthesia · doi:10.1093/bja/aem128 · Cited by 286
Axis II psychopathology in individuals with traumatic brain injury
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
Cytokines and Metabolic Dysfunction After Severe Head Injury
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
“The systemic effects include hypercatabolism, hypermetabolism, and a hyper-dynamic state accompanied by an acute phase response (Clifton et al., 1981 ; McClain et al., 1986; Young et al., 1985,1988,1991).”
Traumatic brain injury: pathophysiology for neurocritical care
Kinoshita, K. (2016) · Journal of Intensive Care · doi:10.1186/s40560-016-0138-3 · Cited by 257
“Indeed, the catecholamine surge following systemic insult is directly involved in the regulation of cytokine expression in situations of acute stress [11, 12, 14], producing a worsening clinical condition and, ultimately, a poor outcome [11, 15].”
BackgroundInfluentialBrain-gut axis dysfunction in the pathogenesis of traumatic brain injury
Hanscom, M., Loane, D. J., & Shea‐Donohue, T. (2021) · Journal of Clinical Investigation · doi:10.1172/jci143777 · Cited by 245
“TBI increases sympathetic activity early after injury, instigating a stress response leading to a sympathetic storm (51, 52, 54, 84, 85).”
BackgroundCerebral salt wasting: Truths, fallacies, theories, and challenges
Singh, S. K., BOHN, D. J., Carlotti, A. P. D. C. P., Cusimano, M. D., Rutka, J. T., & Halperin, M. L. (2002) · Critical Care Medicine · doi:10.1097/00003246-200211000-00028 · Cited by 212
“The levels of adrenergic hormones are elevated in patients with major injuries to the brain (32).”
BackgroundDash, P. K., Zhao, J., Hergenroeder, G. W., & Moore, A. N. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2009.10.019 · Cited by 221
“For example, Clifton et al. 74 demonstrated that serum norepinephrine levels, although normal in TBI patients with a Glasgow coma score (GCS) of 14, dramatically increased in comatose patients.”
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
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
Mechanical brain injury: the sympathoadrenal response
Rosner, M. J., Newsome, H. H., & Becker, D. P. (1984) · Journal of neurosurgery · doi:10.3171/jns.1984.61.1.0076 · Cited by 209
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
Battista, A. P. D., Rhind, S. G., Hutchison, M. G., Hassan, S., Shiu, M. Y., Inaba, K., Topolovec‐Vranic, J., Neto, A. C., Rizoli, S. B., & BAKER, A. J. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0500-3 · Cited by 192
“In an effort to restore vital homeostasis in the face of TBI, activation of the sympathetic nervous system (SNS) results in a massive secretion of catecholamines [epinephrine (Epi), norepinephrine (NE)] into the periphery as part of the generalized host stress response to trauma [7–13].”
BackgroundBeta-Blocker Exposure is Associated With Improved Survival After Severe Traumatic Brain Injury
Cotton, B. A., Snodgrass, K., Fleming, S. B., Carpenter, R. O., Kemp, C. D., Arbogast, P. G., & Morris, J. A. (2007) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0b013e31802d02d0 · Cited by 184
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
“Fluid percussion injury results in a massive catecholamine release (Rosner et al., 1984), which is likely to be responsible for the hypertensive response to the injury (Clifton et al., 1981, 1983).”
The predictive value of catecholamines in assessing outcome in traumatic brain injury
Woolf, P. D., Hamill, R. W., Lee, L. A., Cox, C., & McDonald, J. V. (1987) · Journal of neurosurgery · doi:10.3171/jns.1987.66.6.0875 · Cited by 180
Ventricular fluid interleukin-1 activity in patients with head injury.
McClain, C. J., Cohen, D. A., Ott, L. G., Dinarello, C. A., & Young, B. A. (1987) · PubMed · Cited by 161
Traumatic brain injury: a review of pathophysiology and management
Sande, A. A., & West, C. (2010) · Journal of Veterinary Emergency and Critical Care · doi:10.1111/j.1476-4431.2010.00527.x · Cited by 161
Cardiovascular response to severe head injury
Clifton, G. L., Robertson, C. S., Kyper, K., Taylor, A. A., DHEKNE, R. D., & Grossman, R. G. (1983) · Journal of neurosurgery · doi:10.3171/jns.1983.59.3.0447 · Cited by 157
Self-citationPotentiating glymphatic drainage minimizes post-traumatic cerebral oedema
Hussain, R., Tithof, J., Wang, W., Cheetham-West, A., Song, W., Peng, W., Sigurdsson, B., Kim, D., Sun, Q., Peng, S., et al. (2023) · Nature · doi:10.1038/s41586-023-06737-7 · Cited by 169
“Noradrenaline (NA) levels are significantly increased in patients with TBI 2–4 , and the degree of NA elevation correlates with the severity of injury 5 , functional outcome and mortality 6 .”
BackgroundTraumatic Brain Injury and Peripheral Immune Suppression: Primer and Prospectus
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“Given that TBI results in increased circulating levels of catecholamines (65, 66), then lymphocyte retention in lymph nodes may be one mechanism by which to explain the significant reduction in circulating T cells that has been observed following TBI.”
BackgroundSecond Impact Syndrome: Concussion and Second Injury Brain Complications
Wetjen, N. M., Pichelmann, M. A., & Atkinson, J. L. D. (2010) · Journal of the American College of Surgeons · doi:10.1016/j.jamcollsurg.2010.05.020 · Cited by 151
Heterotopic Ossification Revisited
Mavrogenis, A. F., Soucacos, P. N., & Papagelopoulos, P. J. (2011) · Orthopedics · doi:10.3928/01477447-20110124-08 · Cited by 148
Beyond the Brain: Peripheral Interactions after Traumatic Brain Injury
McDonald, S. J., Sharkey, J. M., Sun, M., Kaukas, L., Shultz, S. R., Turner, R. J., Leonard, A. V., Brady, R. D., & Corrigan, F. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6885 · Cited by 152
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
Use of catecholamines in pediatrics
ZARITSKY, A. L., & Chernow, B. (1984) · The Journal of Pediatrics · doi:10.1016/s0022-3476(84)80003-7 · Cited by 142
Post-traumatic neurodegeneration and chronic traumatic encephalopathy
Daneshvar, D. H., Goldstein, L. E., Kiernan, P. T., Stein, T. D., & McKee, A. C. (2015) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2015.03.007 · Cited by 130
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
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
Catecholamines as outcome markers in isolated traumatic brain injury: the COMA-TBI study
Rizoli, S. B., Jaja, B. N. R., Battista, A. P. D., et al. (2017) · Critical Care · doi:10.1186/s13054-017-1620-6 · Cited by 125
“Alert patients (GCS 14) had normal NE values while patients in coma had levels up to seven times above normal [15].”
Beta-Blockers in Isolated Blunt Head Injury
Inaba, K., Teixeira, P. G., David, J., Chan, L. S., Salim, A., Brown, C., Browder, T. D., Beale, E., Rhee, P., & Δημητριάδης, Δ. (2007) · Journal of the American College of Surgeons · doi:10.1016/j.jamcollsurg.2007.10.005 · Cited by 121
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
Bruder, N. J., Raynal, M., Pellissier, D., Courtinat, C., & François, G. (1998) · Critical Care Medicine · doi:10.1097/00003246-199803000-00033 · Cited by 110
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
“…the oxidative stress in our patients with indirect neurotrauma, mild and severe brain injury could be explained not only in terms of injury severity-related neutrophil activity, but also as a consequence of distinct metabolic and endocrine changes, especially sympathetic discharge (Clifton, 1981).”
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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
“Clifton and colleagues showed that patients with higher levels of catecholamines in blood had worse neurological outcomes, which was likely due to damage arising from the manifestations of PSH seen in the central nervous system (Clifton et al., 1981).”
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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 104
“Studies have suggested for some time that dopamine plays a role in CNS plasticity after brain injury (Clifton et al., 1981), reflected in a reduction in dopamine betahydroxylase (DBH) immunoreactivity (Zhu et al.”
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
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
Paroxysmal Sympathetic Hyperactivity After Acute Brain Injury
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
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
“Concurrent elevations in sympathetic drive have been demonstrated after both cerebral haemorrhage (Naredi et al. 2000) and traumatic brain injury (Clifton et al. 1981, Hinson & Sheth 2012), and there is a positive association between hypertension severity and poor patient outcome (Willmot et al.…”
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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
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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
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BackgroundCardiomyopathy in Soman and Sarin intoxicated rats
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
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
“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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Heffernan, D. S., Inaba, K., Arbabi, S., & Cotton, B. A. (2010) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0b013e3181f2d3e8 · Cited by 82
“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
Krakau, K., Omne-Pontén, M., Karlsson, T., & Borg, J. (2006) · Brain Injury · doi:10.1080/02699050500487571 · Cited by 85
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 81
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
Kobori, N., Clifton, G. L., & Dash, P. K. (2006) · Journal of Neurotrauma · doi:10.1089/neu.2006.23.1094 · Cited by 80
“Studies in humans have shown that circulating norepinephrine levels correspond to the level of injury with comatose patients having serum norepinephrine levels as high as seven times normal (Clifton et al., 1981).”
Self-citationInfluence of Alcohol on Mortality in Traumatic Brain Injury
Opreanu, R. C., Kuhn, D. M., & Basson, M. D. (2010) · Journal of the American College of Surgeons · doi:10.1016/j.jamcollsurg.2010.01.036 · Cited by 80
Effects of Catecholamines on Oxygen Consumption and Oxygen Delivery in Critically III Patients
Chioléro, R. L., Flatt, J. P., Revelly, J., & Jéquier, E. (1991) · CHEST Journal · doi:10.1378/chest.100.6.1676 · Cited by 73
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 87
Purkayastha, S., Stokes, M. A., & Bell, K. R. (2019) · Brain Injury · doi:10.1080/02699052.2019.1631488 · Cited by 86
“Exaggeration of the SNA and elevated plasma catecholamine levels have been associated with moderate to severe TBI (26).”
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
Skoglund, K., Enblad, P., Hillered, L., & Marklund, N. (2011) · Critical Care Medicine · doi:10.1097/ccm.0b013e31822d7dbd · Cited by 68
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
Walia, S. K., & Sutcliffe, A. J. (2002) · Injury · doi:10.1016/s0020-1383(02)00053-0 · Cited by 72
“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
“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…”
MethodCognitive effects of antipsychotic agents in persons with traumatic brain injury
Stanislav, S. W. (1997) · Brain Injury · doi:10.1080/026990597123494 · Cited by 70
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
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
Early propranolol after traumatic brain injury is associated with lower mortality
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
“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
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 70
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
“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
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
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
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
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
“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
Yang, S., Zhang, S., & Wang, M.-L. (1995) · Surgical Neurology · doi:10.1016/0090-3019(96)80243-6 · Cited by 61
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
Hyponatremia and Brain Injury: Historical and Contemporary Perspectives
Kirkman, M. A., Albert, A. F., Ibrahim, A. G., & Doberenz, D. T. (2012) · Neurocritical Care · doi:10.1007/s12028-012-9805-y · Cited by 60
“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
Young, B. A., Ott, L. G., Yingling, B., & McClain, C. J. (1992) · Journal of Neurotrauma · doi:10.1177/089771519200901s36 · Cited by 58
“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
Grände, P. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00315 · Cited by 57
“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
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
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 51
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
“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
“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
Marklund, N. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00540 · Cited by 46
O’Meara, A. I., Sequeira, J., & Ferguson, N. M. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.00118 · Cited by 47
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
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
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
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
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
“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
Metadata
- 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 › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › 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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