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Abstract Therapeutic hypothermia for acute brain injury is the intentional lowering of body temperature, with the objective of reducing tissue damage in the central nervous system. Modern use of therapeutic hypothermia as a neuroprotective strategy began in the 1940s with the work of Fay, who reported the first series of patients with traumatic brain injury who were treated using hypothermia. Therapeutic hypothermia has become a standardized method of care for improving neurological results after cardiac arrest. This approach has been used since the publication of two randomized studies with positive outcomes, each of which used 33°C for 12 h to 24 h [2,3], respectively.(Bernard SA et al, 2002) Recently, a new randomized trial revisited the question of target temperature and was unable to demonstrate any difference in mortality or in adverse neurologic outcome in patients treated at 33°C compared with those treated at 36°C . Therapeutic hypothermia has been historically classified into: mild (34.5–36.5°C), moderate (34.5–32°C), marked (28–32°C) and profound hypothermia (<28°C) . (Nielsen N et al, 2013) Actually, there is a recommendation from five professional societies replaced the term “therapeutic hypothermia” with the term “target temperature management” (TTM) , which implies a broad range for controlling body temperature; TTM can also be applied to normothermia using a similar approach.(Nunnally ME et al, 2011) Vascular supply of the brain and physiology of cerebral perfusion: The brain is supplied by the two internal carotid and the two vertebral arteries. The four arteries lie within the subarachnoid space, and their branches anastomose on the inferior surface of the brain to form the circle of Willis, When the circle is complete, it contains a posterior communicating artery on each side and an anterior communicating artery, The two vertebral arteries form a single midline Basilar artery after passing through foramen magnum. The Venous drainage of the brain and coverings includes the veins of the brain |