Definition: disregulated sympathetic response seen in patients with severe acute brain injury - Most common with TBI (~20% of pt) > anoxic-ischemic brain injury > encephalitis, vasculitis, fat embolism, hypoglycemia, etc Pathophys: possibly due to disconnection between cortical inhibitory areas and sympathetics centers in diencephalon, brainstem, and spinal cord Clinical features: - Rapid onset w/ external stimulation, such as endotracheal tube suctioning, loud noises, repositioning, and urinary retention - Episodes are paroxysmal: - lasting 20-30 min and self resolve - appearing most often around 10 d after brain injury Diagnosis and Differentials: - Diagnosis starts with counting the signs of sympathetic activation below w/o parasympathetic signs of contradicting symptoms that could indicate another origin of sympathetic activation: - PE - hypoxic - Sepsis - hypotensive - ↗ ICP - bradycardia, slowed breathing ([[Cushing Triad]]) - Tonic seizure - no tachypnea, diaphoresis - Acute pain - physical source - Alcohol withdrawal - tremor, agitation, less paroxysmal ![[736B4990-D932-4625-A6C8-D401CD7CD21B.png | 600]] Tx: - Abort: IV morphine (2 mg) - Prevention: Gabapentin (starting dose 100 to 300 mg thrice daily) with a noncardioselective beta blocker (eg, propranolol, at a starting dose of 10 mg thrice daily) and/or clonidine at a starting dose of 0.1 mg twice daily to prevent recurrent episodes - ICU alt: dexmedetomidine for initial prevention and control - Refractory: Intrathecal baclofen Full list of drugs for reference: ![[3C0BC6F4-E187-4E04-860A-1B7629C7A60E.png]] ![[9150A70B-758A-40A6-B84E-619E5C581EE5.png]]