The brain and the lungs interact early and rapidly when hit by a disease process. Often well tolerated by the healthy brain, an impaired respiratory function may deteriorate further a "sick" brain. Hypoxemia is a prognostic factor in the brain-injured patients. At the opposite, an acute brain damage early impacts the lung function. Local brain inflammation spreads rapidly to the lung. It initiates an immunological process weakening the lungs and increasing its susceptibility to infection and mechanical ventilation. Sometimes this process is preceded by a swelling lesion, known as neurogenic pulmonary oedema, resulting from an sympathetic overstimulation which usually follows an intense and brutal surge of intracranial pressure. The management of brain-injured patients has to be directed toward the protection of both the brain and lung. Neuronal preservation is crucial, because of the lack of regenerative potential in the brain, unlike the lung. A compromise must be obtained between the cerebral and pulmonary treatments although they may conflict in some situations.