Severe brain injury (SBI) is one of the world's leading causes of death and disability in young adults.~Its impact on cerebral vascularization is well known. At the systemic level, it induces transient dysfunctions that can develop into severe failures, even in cases of isolated SBI. Studies on a mouse model of SBI show alterations in peripheral vascular reactivity that persist over time and are linked to endothelial dysfunction, the mechanism of which is a decoupling of endothelial NO synthase in a context of systemic inflammation. However, no data are available regarding the peripheral vascular consequences of SBI in humans.~The main objective of this prospective, monocentric, pathophysiological study is to determine whether the postocclusive hyperaemic response at the anterior surface of the contralateral forearm to the most injured cerebral hemisphere differs between patients with severe brain injury and patients with severe trauma without associated head injury matched on sex and age (+/- 5 years), by studying the amplitude of post-occlusive hyperaemia (maximum amplitude expressed as percentage of vasodilatation and area under the curve : AUC) as a function of the group.
Severe brain injury (SBI) is one of the world's leading causes of death and disability in young adults, but its peripheral vascular consequences in humans are poorly understood.~This prospective, monocentric, pathophysiological study aims to investigate differences in vasoreactivity in the anterior aspect of the contralateral forearm at the most injured cerebral hemisphere between patients with severe head trauma and patients with severe trauma without associated brain injury matched on sex and age (+/- 5 years).