Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that occurs after traumatic brain injury (80%) and after anoxic brain injury (10%). It is characterized by autonomic instability with episodes of hypertension, tachycardia, diaphoresis, hyperthermia and motor posturing. Why it occurs is poorly understood, it has been theorized to be due to the loss of inhibitory pathways causing excitation with minimal stimuli. Treating PSH can be challenging yet crucial as paroxysms need to be controlled to prevent secondary brain injury. We will describe the case of an unfortunate young male who suffered anoxic brain injury of unknown etiology.CASE PRESENTATION: A 23-year old male was found unresponsive in his car. He was admitted to the ICU for acute metabolic encephalopathy with concerns of possible drug intoxication (seizures, carbon monoxide poisoning and CNS infection also being on the differential). Urine toxicology was only positive for marijuana. Carboxyhemoglobin was 8.3%, but patient was too unstable to be transferred to a hyperbaric chamber. Patient required intubation and pressor support. MRI showed anoxic brain injury. Sedation was weaned off the second day and patient suffered an episode of hypertension, tachypnea, tachycardia, diaphoresis and decerebrate posturing followed by flash pulmonary edema. Patient had a prolonged hospital course further complicated by medical emergency events in the setting of PSH with multiple readmissions to the ICU, but eventually exhibited significant neurological recovery. DISCUSSION: In this case, we observed a young man with acute anoxic brain injury who developed PSH. Due to the symptoms, initial treatments were aimed at controlling seizures and infections. The patient was treated with Keppra as well as broadspectrum antibiotics, but continued to exhibit sympathetic surges. During the first event, he developed end-organ damage (flash pulmonary edema) requiring increased ventilatory support. Though there is no standardized treatment for PSH, we initiated therapy described in the literature with success. The patient was started on Propranolol, Gabapentin, Morphine and Versed with good response.CONCLUSIONS: When treating patients with traumatic or anoxic brain injury, it is important to keep PSH on the differential. PSH symptoms overlap with many other conditions such as septicemia, seizures, or hydrocephalus making it easily underdiagnosed. Earlier recognition of adrenergic surges leads to better symptom control. We would also recommend better stimulation control as light tactile stimuli could drive our patient into surges. With our patient, we used Propranolol, Gabapentin, Morphine and Versed with adjustment of regimen as needed. Finally, we stress the importance of a complete neurological exam off of all sedation when possible, as our patient, who initially had an extremely poor prognosis, was able to recover neurological function.