الفهرس 
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Abstract
Traumatic brain injury is a leading cause of death and disability and a major public health concern. Although the severity of brain damage due to the traumatic impact accounts for the majority of early mortality after TBI, secondary damage to the injured brain can occur as a result of hypoxia, hypotension, hyper and hypocarbia, increased intracranial pressure, and hyperglycemia, all leading to a poor outcome (Faul M et al., 2010).
Propofol has a relatively rapid onset and short duration of action, which allows rapid assessment of neurological status. It is administered by continuous infusion and can be given for long periods with little change in its pharmacokinetic profile. It has no active metabolites. The duration of action is dependent on the redistribution of propofol into the peripheral tissues –emergence is slightly prolonged after infusions of more than 12 hours. There is less certainty relating to seizure control with propofol, mainly because changes in cerebral concentrations at induction or emergence from sedation may induce seizure-like phenomena. However, propofol infusions are regularly and successfully used in the management of status epilepticus. A number of problems have been associated with propofol, including precipitous cardiovascular collapse and propofol infusion syndrome. Propofol is not recommended in hypothermic patients due to the risk of hyperlipidaemia (Zaccheo et al., 2008).