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
Pharmacotherapy
- Antipsychotic agents: via dopamine pathways
- Could cause neuroleptic malignant syndrome (treat w/ dantrolene/beta blockers)
| block D2 receptors (and H, 𝛂1, cholinergic receptors) |
| Haldol can prolong PTA and slow motor recovery. Avoid in TBI! |
|
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 |
| 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 |
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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.