After initial stabilization and when intracranial pressure is controlled, the use of benzodiazepines in the acute phase of traumatic brain injury should be limited to specific medical indications, such as alcohol withdrawal. In animal models of acute TBI, benzodiazepines have been associated with slowed or halted recovery. Moreover, benzodiazepines have adverse effects on cognition, and can cause respiratory depression, paradoxical agitation, and anterograde amnesia. Non-pharmacologic interventions are essential components of the management of agitation after TBI. Beta blockers, such as propranolol, are first line pharmacotherapeutic agents, and anticonvulsants can also be used to decrease agitated behaviours.
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