Subtype of delirium occurring during PTA characterized by excesses of behavior like aggression, akathisia, disinhibition and/or emotional lability

Usually with frontotemporal lesions (affecting arousal, attention, executive control, memory, limbic behavioral functions)

Usually occurs as patients become more responsive in early stages of recovery

Usually lasts 1-14 days but can last longer


First Line

safe, structured, low-stimulus environment

  • Quiet private room, remove lines/tubes as much as possible
  • Floor bed with padded side panels, sitter, avoid taking patient off unit
  • One person speaking, one topic/idea at a time, maintain familiar staff
  • Allow patient to pace or move in bed with supervision, tolerate some restlessness

Second Line


  • Antipsychotic agents: via dopamine pathways
  • Could cause neuroleptic malignant syndrome (treat w/ dantrolene/beta blockers)
Typical Antipsychotics
block D2 receptors (and H, 𝛂1, cholinergic receptors)
Haldol can prolong PTA and slow motor recovery.
Avoid in TBI!
Atypical Antipsychotics
less D2 blockage, more serotonin blockage (5-HT2)
Less likely motor side effects but frequent metabolic side effects
risperidone (Risperdal) least anticholinergic, can be stimulating, can impede cognitive recovery after TBI
quetiapine (Seroquel) sedating, less motor SEs, prolongs QT; usually start at 25-50mg qHS, can titrate up by 25-50mg every 1-2 days to 300mg/day but monitor QTc closely
olanzapine (Zyprexa) sedating, metabolic SEs, acute IM form; usually start at 2.5-5mg qHS, can titrate up by 5-10mg every 1-2 days; IM can be from 5-10mg, 2h after initial dose and 4h after 2nd dose should be allowed to evaluate response (max 20mg/day
Can impair motor recovery, cause transient recurrence of hemiparesis or paradoxical agitation, increase confusion in those emerging from PTA
midazolam, lorazepam (short acting) lowest dose possible, only if necessary
Have best evidence for efficacy in treating post-traumatic agitation
No effect on motor recovery, can cause lethargy/depression at high doses
propranolol 10-20 mg q6-8h
Anticonvulsants (mood stabilizers)
valproic acid (Depakote, Depakene) 1250-1800 mg/day
carbamazepine (Tegretol) 400-800 mg/day
oxcarbamazepine (Trileptal)
amitriptyline (Elavil) 25-150 mg/day
sertraline (Zoloft) 25-300 mg/day
trazodone 25-300 mg/night
buspirone 10-45 mg/day
bupropion 150 mg/day
  • References

    Elovic E, Baerga E, Galang GF, Cuccurullo SJ, Reyna M, Malone RJ. Physical Medicine and Rehabilitation Board Review. 3rd ed. New York, NY: Demos Medical; 2015. Chapter 2, Traumatic Brain Injury. P.96-146.

    Wagner AK, Arenth PM, Kwasnica C, Rogers EH, Braddom RL. Physical Medicine and Rehabilitation. 4th ed. Philadelphia, PA: W.B. Saunders Company; 2011. Chapter 49, Traumatic Brain Injury. P.1133-1175.

    Feeney DM, Gonzalez A, Law WA. Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex injury. Science. 1982;217(4562):855–857.

    Phelps TI, Bondi CO, Ahmed RH, Olugbade YT, Kline AE. Divergent long-term consequences of chronic treatment with haloperidol, risperidone, and bromocriptine on traumatic brain injury-induced cognitive deficits. J Neurotrauma. 2015;32(8):590-7.

    Plantier D, Luaute J, the SOFMER group. Drugs for behavior disorders after traumatic brain injury: Systematic review and expert consensus leading to French recommendations for good practice. Annals of Physical and Rehabilitation Medicine. 2016;59(1):42-57.