Background. Stress cardiomyopathy is common after subarachnoid haemorrhage but has been scarcely described after traumatic brain injury. Methods. Mono-centric longitudinal study in moderate to severe traumatic brain injury (Glasgow coma score ≤ 12). Evaluation of global longitudinal strain and 2-dimension trans-thoracic echography at day-1, day-3 and day-7. The primary outcome was the incidence of stress cardiomyopathy assessed with global longitudinal strain. Secondary outcomes were the relationship between global longitudinal strain and mortality, plasma levels of metanephrine and normetanephrine in patients with traumatic brain injury and subarachnoid haemorrhage to explore the mechanisms of stress cardiomyopathy. Results. We included 100 patients from March 2014 to August 2017. Twenty (20%) patients died in the intensive care unit. At day 1, global longitudinal strain (-20.3(±3.6)%) and left ventricular ejection fraction (65.9 (±10.8)%) were preserved. Nine (9%) patients displayed impaired global longitudinal strain (-13.3[-14.5/-11.6]%) at baseline, with significant improvement at day-3 and day-7 (p<0.0001), compatible with stress cardiomyopathy. There was a slight global longitudinal strain improvement at day-3 in the overall population ((-22.2 (± 3.6)%, p=0.004), but was similar to baseline at day-7 (-20.7(± 3.3)%). Global longitudinal strain was not related to mortality (p=1). In 15 subarachnoid haemorrhage and 15 traumatic brain injury patients matched with age and severity, there were no differences in baseline normetanephrine or metanephrine plasma levels. Conclusions. Stress cardiomyopathy could occur after traumatic brain injury, but global longitudinal strain remains preserved. The raised baseline metanephrine and normetanephrine is comparable in traumatic brain injury and subarachnoid haemorrhage patients. Thus, sympathetic hyperactivation is probably not the only mechanism involved in stress cardiomyopathy.