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Updated: May 20, 2026

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
Published on: May 27, 2022
Paroxysmal Sympathetic Hyperactivity in Non-traumatic Brain Injury: A Retrospective Analysis From the Intensive Care
Jitendra S Chahar1, Sangam Yadav1, Sai Saran1
1Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, IND.
Background:
Paroxysmal sympathetic hyperactivity (PSH) can occur in comatose patients with a history of non-traumatic brain injury. In the intensive care unit, it is very challenging to diagnose such a condition, as there are a lot of masquerades.
Methods:
This was a retrospective study, which screened case records of adult patients (age > 18 years), referred to a 26-bed intensive care unit of a tertiary care academic university, admitted with a comatose state, either post-cardiac arrest status with presumptive diagnosis of hypoxic ischemic brain injury, or patients with suspected meningo-encephalitis for a period of one year. Patient case files suggestive of a history of traumatic brain injury, stroke, epilepsy, and autonomic dysfunction were excluded. Case files with a Paroxysmal Sympathetic Hyperactivity-Assessment Measure (PSH-AM) score ≥17 were included. The case files were reviewed for a period of two weeks starting from the day PSH was diagnosed, and the outcome was assessed in terms of changes in PSH-AM scores and Glasgow Outcome Scale Extended (GOS-E) at ICU discharge.
Results:
The prevalence of PSH was 17% in comatose patients with hypoxic ischemic encephalopathy (n = 04) and acute meningo-encephalitis (n = 03). There were seven patients with a diagnosis of probable PSH (PSH-AM score ≥17). The median age of the study cohort was 41 years (35-48 years). The median value of severity of illness at ICU admission as assessed by the Acute Physiology and Chronic Health Evaluation II (APACHE II) was 19 (13-21). The median PSH-AM score was 20 (18-21) at the time of diagnosis of PSH, which was 38 days (21-42 days) from the neurological insult. The PSH score reduced to 5 (3-14) after two weeks of treatment (p < 0.001) with propranolol and clonidine. The median GOS-E of the study population was 2 (2-3).
Conclusion:
A high index of suspicion should be kept for diagnosing PSH in patients with non-traumatic brain injury, particularly those with hypoxic brain injury and encephalitis. Episodic tachycardia, hypertension, diaphoresis, and posturing are important features to suspect PSH in comatose patients with a history of non-traumatic brain injury after ruling out other mimics in the ICU, such as sepsis. The PSH-AM score can be helpful in screening for PSH in such patients. Early identification and management of PSH in such critically ill patients can reduce the number of medical interventions.
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