Multimodal treatment strategies for TBI patients – Why do we need them?

Traumatic brain injury (TBI) affects over 10 million people each year, causes more lost productive years of life than any other disease and is the leading cause of death and disability in people under the age of 45. In particular, cognitive deficits and depression are frequent consequences. Stringent treatment and rehabilitation concepts are crucial. In addition to the primary injury, secondary damage is a focus of current research and treatment strategies: following the trauma, increased glutamate levels lead to excitotoxicity, cellular and humoral immune response is strongly activated and the integrity of the blood-brain barrier (BBB) is disrupted.

The consequences are excessive neuroinflammation, unbridled excitation spread over the cortex, excessive cellular influx of Ca++ and Na+ with cerebral edema formation, disruption of the energy balance, apoptosis and cell death. However, there are also regenerative processes in the injured brain: neurotrophic factors initiate repair of damaged cell membranes, sealing of the BBB and protection of the mitochondrial energy supply; Neurogenesis, angiogenesis and neuroplasticity are stimulated.

Current guidelines (e.g. Brain Trauma Foundation) provide clear recommendations for surgery, emergency and intensive care treatment. They essentially focus on limiting intracranial pressure, maintaining cerebral perfusion, reducing cerebral oxygen consumption and the homeostasis of the organism in the acute and post-acute phases. Nevertheless, the use of neurotrophic substances is controversial, despite promising preclinical and clinical data. This presentation discusses the use of the most interesting clinically available substances and provides current evidence for higher survival rates, shorter intensive care stays and better cognitive outcomes.