Introduction. Paroxysmal sympathetic hyperactivity (PSH) can occur as a result of brain injury, hypoxic brain damage, acute cerebrovascular accident (ACVA). The clinical picture of PSH is caused by excessive sympathetic activity and includes transient paroxysms of tachycardia, hypertension, hyperventilation, hyperthermia, and diaphoresis. PSH is a neurological emergency, which in the vast majority of cases is a diagnosis of exclusion. Lack of adequate detection and treatment of the disease leads to a high mortality rate. The diagnosis is exclusively clinical, so other pathologies must be excluded. Currently, the most widely accepted diagnostic criteria for PSH are the criteria proposed by Baguley et al.
Case description. Patient D., 29 years old, was hospitalized with a diagnosis of middle cerebral artery stroke. The patient had attacks which were characterized by tachycardia, hypertension, tachypnea with asynchrony with the ventilator, diaphoresis and hypertension every day with a frequency of 2-3 times per day and were ending approximately 30-40 minutes after the onset. The diagnosis of PSH was established according to the score on the scale proposed by Baguley et al., 25 points (17 or more points – a probable diagnosis of PSH).
Conclusions. It is believed that the cause of PSH is a violation of the inhibition function of the cortex on the brain structures located below, as a result of which paroxysms of sympathetic activation occur, manifested by tachycardia, hypertension, hyperventilation, diaphoresis, and hyperthermia. In this clinical case, resolution of paroxysms was observed faster with the combination of morphine and propofol. An important aspect of therapy is adequate rehydration therapy to compensate for fluid losses due to hyperthermia and diaphoresis, as well as the administration of beta-blockers on an ongoing basis