The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the "blast injury" theory or "double hit" model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.

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Worldwide, traumatic brain injury (TBI) comprises a combined incidence rate for all ages of approximately 350 per 100,000 person-years and is a leading cause of death and disability in trauma patients 1,2) . The presentation of TBI varies from mild alterations of consciousness to a comatose state and death 3) . However, despite the existence of many classification systems, the simplest includes mild, moderate, and severe TBI, in which the nature of the injury and the impact on the patient's clinical condition is considered 4) . In the last decade, a clear trend has been demonstrated towards deterioration in patients with severe TBI, in which the whole brain is affected precisely because of the characteristics and degree of injury. This deterioration may be associated with a loss of autoregulation due to the lack of reactivity of cerebral vascular pressure, resulting in hyperemia, interstitial edema and subsequent intracranial hypertension (ICH) 5,6) .Normal intracranial pressure in adults is less than 15 mm Hg, values that remain above 20 mm Hg are considered pathological and are an indication for intensified treatment in patients with TBI 7) . It is important to consider that ICH can result from primary injury (hematoma expansion) or secondary damage (water accumulation, impaired autoregulation, ischemia, and contusion expansion). This is associated with high mortality rates, so multiple early, stepwise, and rescue management strategies have been proposed for its control, which is aimed at preventing secondary injury by avoiding hypotension, hypoxia and maintaining adequate cerebral perfusion pressure (CPP). Targeted treatment is essential and may include cerebrospinal fluid (CSF) drainage, use of hyperosmolar therapies, induction of hypothermia, hyperventilation, administration of barbiturates, or performance of decompressive surgery 2,8) .Therapeutic hypothermia (TH) is one of the few neuroprotectants that has moved from preclinical work to clinical use. For example, it was previously used to prevent brain damage during cardiac surgical procedures, but more recently it has also been used to improve both neurological and physical out-