Information is provided from the basic and clinical sciences on the mechanisms damaging the brain from trauma or ischemia. New aspects involve the endoplasmic reticulum, mitochondrial failure, pathobiology of axonal injury, molecular signals activating glial elements, or the emerging therapeutical role of neurotrophins. Experimental issues involve a better analysis of the ischemic penumbra, the salvagable tissue. Therapeutic contributions reach from the environmental influence to gene expression, including neuroprotection, such as hibernation - mother nature's experiment - or hypothermia which is reported to induce cell swelling. Treatment issues deal also with thrombolysis and combination therapies, or with the clearance of adverse blood components - LDL/fibrinogen - by a novel procedure using heparin. Other highlights are discussing the specificities of pediatric vs. adult brain trauma, or the evolving role of the Apolipoprotein-E e4 gene in severe head injury. An update is also provided on an online assessment of the patient management during the pre- and early hospital phase in Southern Bavaria. The empirical observation of neuroworsening is analyzed in further details, whether this is a specificity autonomously driving the posttraumatic course. Finally, the unsolved question why drug trials in severe head injury have failed so far in view of the promising evidence from the laboratory is subjected to an expert analysis.

The international interdisciplinary gathering of top of secondary brain damage in brain trauma, as ac- level clinical and laboratory scientists in Mauls, Italy knowledged from the beginning of these workshops in has developed from its beginning in 1984into a fruitful Mauls, the significance of inflammation is all but clear. tradition where worldwide experts active and knowl- Although inflammatory phenomena are seen in trauma edgeable in cerebral ischemia and trauma convene for and ischemia ofthe brain, as activation ofwhite blood update and exchanges of their most recent clinical and cells with emigration into the tissue presumably en- experimental findings and concepts. These meetings hancing damage, inflammatory cells may have benefi- have, of course, experienced shifts in emphasis from cial properties as well. Thechapter on the Janus-faceof the past until now, corresponding to the most actual inflammation isanalyzing this ambiguity. developments, which were fascinating clinicians and The exploration of novel cell-biological mechanisms laboratory scientists alike. The current Supplement of on a molecular or more systemic basis causing apop- Acta Neurochirurgica is an example in case. Its virtue totic cell death, inflammation, or regeneration, provide as before is that authors contribute articles in a review- useful objectives for therapeutical interventions ex- like manner on their own field of research, according pected to be more specific than the present treatment to the platform presentations at the meeting as indis- modalities.