Clinical and laboratory correlation in patients with consequences of traumatic brain injury
DOI:
https://doi.org/10.15587/2313-8416.2015.48249Keywords:
consequences of traumatic brain injury, apoptosis, necrosis, leukocytesAbstract
The aim of this study was to establish main peculiarities of apoptosis of peripheral blood leukocytes in patients with traumatic brain injury consequences of varying severity under conditions of disease progression
Methods. In 220 patients with the effects of light (71), moderate (59) and hard (90) TBI and the catamnesis of trauma in the age from 1 to 30 years percentage of peripheral blood leukocytes in stage of apoptosis (ANV +) and necrotic (PI +) and the level of reactive oxygen species (ROS +) was explored by flow cytofluorometry method. The control group consisted of 30 people representative by age and sex. Neurological status was assessed by Neurological Outcome Scale for Traumatic Brain Injury (NOS-TBI), cognitive status - Montreal scale for cognitive deficit (Mosa), the level of anxiety and depression – by the HADS scale
Results. Patients with TBI consequences of varying severity established significant growth indicators characterizing the level of necrosis and apoptosis of peripheral blood leukocytes, and increase the percentage of cells containing active oxygen species. Reliable dependence of indicators RI + ANV + peripheral blood leukocytes and ROS + on patient's age, duration and type of injury was not found
Conclusions. Conditioned upon progression of neurological deficit (accession of extra-pyramidal symptoms, occurrence and progression of cognitive disorders, etc.) significantly higher values RI + ANV + peripheral blood leukocytes and ROS + were found
References
McIntosh, T. K., Saatman, K. E., Raghupathi, R., Graham, D. I., Smith, D. H., Lee, V. M., Trojanowski, J. Q. (1998). The Dorothy Russell Memorial Lecture* The molecular and cellular sequelae of experimental traumatic brain injury: pathogenetic mechanisms. Neuropathology and Applied Neurobiology, 24 (4), 251–267. doi: 10.1046/j.1365-2990.1998.00121.x
Faul, M., Xu, L., Wald, M. M., Coronado, V. G. (2010). Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths 2002–2006. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.
Faden, A. I. (1996). Pharmacologic treatment of acute traumatic brain injury. JAMA: The Journal of the American Medical Association, 276 (7), 569–570. doi: 10.1001/jama.276.7.569
Weaver, S. M., Chau, A., Portelli, J. N., & Grafman, J. (2012). Genetic Polymorphisms Influence Recovery from Traumatic Brain Injury. The Neuroscientist, 18 (6), 631–644. doi: 10.1177/1073858411435706
Ramlackhansingh, A. F., Brooks, D. J., Greenwood, R. J., Bose, S. K., Turkheimer, F. E., Kinnunen et. al. (2011). Inflammation after trauma: Microglial activation and traumatic brain injury. Annals of Neurology, 70 (3), 374–383. doi: 10.1002/ana.22455
Stoica, B. A., Faden, A. I. (2010). Cell death mechanisms and modulation in traumatic brain injury. Neurotherapeutics, 7 (1), 3–12. doi: 10.1016/j.nurt.2009.10.023
Miñambres, E., Ballesteros, M. A., Mayorga, M., Marin, M. J., Muñoz, P., Figols, J., López-Hoyos, M. (2008). Cerebral Apoptosis in Severe Traumatic Brain Injury Patients: An In Vitro, In Vivo, and Postmortem Study. Journal of Neurotrauma, 25 (6), 581–591. doi: 10.1089/neu.2007.0398
Gardner, R. C., Yaffe, K. (2015). Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience, 66, 75–80. doi: 10.1016/j.mcn.2015.03.001
Cheng, G., Kong, R., Zhang, L., Zhang, J. (2012). Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies. British Journal of Pharmacology, 167 (4), 699–719. doi: 10.1111/j.1476-5381.2012.02025.x
De Calignon, A., Fox, L. M., Pitstick, R., Carlson, G. A., Bacskai, B. J., Spires-Jones, et al. (2010). Caspase activation precedes and leads to tangles. Nature, 464 (7292), 1201–1204. doi: 10.1038/nature08890
Christofferson, D. E., Yuan, J. (2010). Necroptosis as an alternative form of programmed cell death. Current Opinion in Cell Biology, 22 (2), 263–268. doi: 10.1016/j.ceb.2009.12.003
Wang, H.-C., Yang, T.-M., Lin, Y.-J., Chen, W.-F., Ho, J.-T., Lin, et al. (2014). Serial Serum Leukocyte Apoptosis Levels as Predictors of Outcome in Acute Traumatic Brain Injury. BioMed Research International, 2014, 1–11. doi: 10.1155/2014/720870
Cosentino, M., Marino, F., Bombelli, R., Ferrari, M., Lecchini, S., Frigo, G. (1999). Endogenous catecholamine synthesis, metabolism, storage and uptake in human neutrophils. Life Sciences, 64 (11), 975–981. doi: 10.1016/s0024-3205(99)00023-5
Calopa, M., Bas, J., Callén, A., Mestre, M. (2010). Apoptosis of peripheral blood lymphocytes in Parkinson patients. Neurobiology of Disease, 38 (1), 1–7. doi: 10.1016/j.nbd.2009.12.017
Lin, W.-C., Tsai, N.-W., Huang, Y.-C. et al. (2014). Peripheral Leukocyte Apoptosis in Patients with Parkinsonism: Correlation with Clinical Characteristics and Neuroimaging Findings. BioMed Research International, 2014, 1–7. doi: 10.1155/2014/635923
Hirsch, E. C., Hunot, S. (2009). Neuroinflammation in Parkinson's disease: a target for neuroprotection? The Lancet Neurology, 8 (4), 382–397. doi: 10.1016/S1474-4422(09)70062-6
Bergquist, J., Tarkowski, A., Ekman, R., & Ewing, A. (1994). Discovery of endogenous catecholamines in lymphocytes and evidence for catecholamine regulation of lymphocyte function via an autocrine loop. Proceedings of the National Academy of Sciences, 91 (26), 12912–12916. doi: 10.1073/pnas.91.26.12912
Blandini, F., Sinforiani, E., Pacchetti et al. (2006). Peripheral proteasome and caspase activity in Parkinson disease and Alzheimer disease. Neurology, 66 (4), 529–534. doi: 10.1212/01.wnl.0000198511.09968.b3
Moretti, L., Cristofori, I., Weaver, S. M., Chau, A., Portelli, J. N., Grafman, J. (2012). Cognitive decline in older adults with a history of traumatic brain injury. The Lancet Neurology, 11 (12), 1103–1112. doi: 10.1016/s1474-4422(12)70226-0
Vincent, A. S., Roebuck-Spencer, T. M., Cernich, A. (2014). Cognitive changes and dementia risk after traumatic brain injury: Implications for aging military personnel. Alzheimer’s & Dementia, 10 (3), S174–S187. doi: 10.1016/j.jalz.2014.04.006
Kukull, W. A., Higdon, R., Bowen, J. D., McCormick, W. C., Teri, L., Schellenberg, G. D., Larson, E. B. (2002). Dementia and Alzheimer Disease Incidence. Archives of Neurology, 59 (11), 1737–1746. doi: 10.1001/archneur.59.11.1737
Plassman, B. L., Grafman, J. (2015). Traumatic brain injury and late-life dementia. Handbook of Clinical Neurology, 128, 711–722. doi: 10.1016/B978-0-444-63521-1.00044-3
Wakade, C., Sukumari-Ramesh, S., Laird, M. D., Dhandapani, K. M., Vender, J. R. (2010). Delayed reduction in hippocampal postsynaptic density protein-95 expression temporally correlates with cognitive dysfunction following controlled cortical impact in mice. Journal of Neurosurgery, 113 (6), 1195–1201. doi: 10.3171/2010.3.jns091212
Wilde, E. A., McCauley, S. R., Kelly, T. M. et al. (2010). Feasibility of the Neurological Outcome Scale for Traumatic Brain Injury (NOS-TBI) in Adults. Journal of Neurotrauma, 27 (6), 975–981. doi: 10.1089/neu.2009.1193
MoCA. Available at: http://www.moca-test.orgt
Bjelland, I., Dahl, A. A., Haug, T. T., Neckelmann, D. (2002). The validity of the Hospital Anxiety and Depression Scale. Journal of Psychosomatic Research, 52 (2), 69–77. doi: 10.1016/s0022-3999(01)00296-3
Li, W., Liu, H., Zhou, J.-S. et. al. (2012). Caveolin-1 Inhibits Expression of Antioxidant Enzymes through Direct Interaction with Nuclear Erythroid 2 p45-related Factor-2 (Nrf2). Journal of Biological Chemistry, 287 (25), 20922–20930. doi: 10.1074/jbc.m112.352336
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