[The relevance of the inflammatory response in the injured brain]. / Die Bedeutung der posttraumatischen Entzündungsreaktion im verletzten Gehirn.

Research efforts in recent years have defined traumatic brain injury (TBI) as a predominantly immunological and inflammatory disorder. This perception is based on the fact that the overwhelming neuroinflammatory response in the injured brain contributes to the development of posttraumatic edema and to neuropathological sequelae which are, in large part, responsible for the adverse outcome. While the "key" mediators of neuroinflammation, such as the cytokine cascade and the complement system, have been clearly defined by studies in experimental TBI models, their exact pathways of interaction and pathophysiological implications remain to be further elucidated. This lack of knowledge is partially due to the concept of a "dual role" of the neuroinflammatory response after TBI. This notion implies that specific inflammatory molecules may mediate diverse functions depending on their local concentration and kinetics of expression in the injured brain. The inflammation-induced effects range from beneficial aspects of neuroprotection to detrimental neurotoxicity. The lack of success in pushing anti-inflammatory therapeutic concepts from"bench to bedside" for patients with severe TBI strengthens the further need for advances in basic research on the molecular aspects of the neuroinflammatory network in the injured brain. The present review summarizes the current knowledge from experimental studies in this field of research and discusses potential future targets of investigation.

Locking compression plate with minimally invasive plate osteosynthesis in diaphyseal and distal tibial fracture: a retrospective study of 32 patients.

With the introduction of Locking Compression Plates (LCP), Minimally Invasive Plate Osteosynthesis (MIPO) has become widely used. The plates act as internal fixators in a bridging manner, thus resulting in secondary bone healing. We retrospectively evaluated the healing pattern and the clinical evolution of diaphyseal and distal tibial shaft fractures over two and a half years in 32 patients (6 females, 26 males). Fractures were classified according to AO classification and included all 42A-C, 43A-B and 43C1-2 types. For open fractures, Gustillo Anderson classification was used. Plates consisted of the 4.5mm LCP and 3.5mm LCP-Pilon form plate. Clinical and radiological assessment was performed at 6 weeks, and at 3, 6, 9, and 12 months. Two patients were lost to follow-up. Fracture healing was defined as callus bridging of one cortex, seen on both lateral and posterior-anterior X-ray, and full, painless weight bearing. Ten patients at 3 months, 23 at 6 months, and 27 at 9 months met the criteria for a healed fracture. Plate bending was observed in one patient and called for re-operation at 5 months. Two patients required re-operation at 13 months secondary to pseudoarthrosis. Though MIPO seems more advantageous for soft tissue and bone biology, prolonged healing was observed in simple fracture patterns when a bridging plate technique was used.