Neuroimaging of Traumatic Brain injury

Traumatic Brain Injury (TBI) is a frequent disease and a global burden both in western countries and the third world. Children and adolescents are often affected and TBI is still one of the leading causes of death among them. Socioeconomic burden is considered very high, not only from direct costs of hospitalisation but especially indirect costs, caused by the impairments due to the injury. To make things worse, there is no established (pharmaco)therapy available.Pathophysiology is highly complex, with many different processes that lead to immediate primary and subsequently secondary damage. The primary biomechanic trauma is a highly heterogeneous injury that occurs directly after the incident and causes vascular, neuronal, axonal and glia damage. From those primary injuries, secondary damage develops as a direct result or independently because of delayed processes. Secondary injuries are, among many others, e.g. deficits in perfusion and blood flow, increased intracranial pressure and inflammatory processes. This often causes lifelong impairments, especially of cognitive function like attention, memory and learning. This has been shown to have a dramatic impact on quality of life for adults, however, for children and adults it is considered to be devastating due to the higher relevance of the affected cognitive functions for the later life. Additionally, TBI increases the risk to develop brain tumors in later life.

Changes of acetylcholinesterase (part of the cholinergic neurotransmission) activity in TBI patients compared to healthy volunteers. More red areas mean stronger changes. FromÖstberg A, et al.; Cholinergic dysfunction after traumatic brain injury: preliminary findings from a PET study. Neurology. 2011 22;76(12):1046-50. TBI: Changes of acetylcholinesterase

​Our goal is therefore to investigate basic processes after TBI in animal models, e.g. changes in neurotransmitter density with in vitro methods like autoradiography and (immuno)histochemistry. This should allow us to identify critical molecular targets that may play crucial roles in the damaging processes after TBI. Employing the radioactive tracer principle allows a later translation into the clinical practice by using Positron-Emission-Tomography as a diagnostic tool.

Basic pathophysiological processes after TBI. TBI: Basic pathophysiological processes


  • Department of Neurosurgery at the University Clinics Leipzig

  • Department of Neurosurgery at the Eberhard-Karls-University Tübingen

  • Institute of Molecular Cell Biology at the Friedrich-Schiller-University Jena

  • Paul-Flechsig-Institute for Brain Research at the University of Leipzig


  • Donat, C.K., Schuhmann, M.U., Voigt, C., Nieber, K., Schliebs, R., Brust, P., 2007. Alterations of acetylcholinesterase activity after traumatic brain injury in rats. Brain Inj 21, 1031-1037; PubMed ID: 17891565

  • Donat, C.K., Schuhmann, M.U., Voigt, C., Nieber, K., Deuther-Conrad, W., Brust, P., 2008. Time-dependent alterations of cholinergic markers after experimental traumatic brain injury. Brain Res 1246, 167-177; PubMed ID: 18848922

  • Donat, C.K., Walter, B., Kayser, T., Deuther-Conrad, W., Schliebs, R., Nieber, K., Bauer, R., Härtig, W., Brust, P., 2010. Effects of lateral fluid percussion injury on cholinergic markers in the newborn piglet brain. Int. J. Developmental Neuroscience, 28(1), 31-8; PubMed ID: 19822201

  • Donat, C.K., Walter, B., Deuther-Conrad, W., Wenzel, B., Nieber, K., Bauer, R., Brust, P., 2010. Alterations of cholinergic receptors and the vesicular acetylcholine transporter after lateral fluid percussion injury in newborn piglets. Neuropathology Applied Neurobiology, 36(3), 225-36; PubMed ID: 19889177

  • Hoffmeister, P.G., Donat, C.K., Schuhmann, M.U., Voigt, C., Walter, B., Nieber, K., Bauer, R., Brust, P., 2011. Alterations of α7 nicotinic receptors in an adult and newborn model of traumatic brain injury. NeuroMolecular Medicine, (1):44-53, PubMed ID: 20857232

  • Voigt, C., Donat, C.K., Härtig, W., Foerschler, A., Arendt, T., Meixensberger, J., Schuhmann, M.U., 2012. Effect of leukotriene inhibitors on evolution of experimental brain contusions.Neuropathol Applied Neurobiology, 38(4):354-66, PubMed ID: 21834945

  • xxxxxxxxxxxxxxxxImpact of 5-lipoxygenase inhibitors on the spatiotemporal distribution of inflammatory cells and neuronal COX-2 expression following experimental traumatic brain injury in rats.

  • Härtig, W., Michalski, D., Seeger, G., Voigt, C., Donat, C.K., Dulin, J., Kacza, J., Meixensberger, J., Arendt, T., Schuhmann, M.U. Brain Res. 2012 Dec 23. doi:pii: S0006-8993(12)01933-6. 10.1016/j.brainres.2012.12.022. PubMed ID: 23268351