From the Guidelines
Beta blockers should be used to manage neurostorming in patients with traumatic brain injury, as they have been shown to potentially reduce mortality and improve outcomes. According to a systematic review and meta-analysis published in the Annals of Surgery in 2017 1, treatment with beta-adrenergic receptor antagonists offers a potentially beneficial approach to blunting the cascade of sympathetic activation after traumatic brain injury. The use of beta blockers, such as propranolol, metoprolol, or labetalol, can help control symptoms of neurostorming, including tachycardia, hypertension, hyperthermia, tachypnea, and diaphoresis.
Some key points to consider when using beta blockers for neurostorming include:
- Starting with a low dose and titrating up as needed to control symptoms
- Monitoring vital signs closely to avoid bradycardia and hypotension
- Using caution in patients with asthma, heart block, or heart failure
- Considering alternative medications, such as alpha-2 agonists, benzodiazepines, or opioids, for severe cases
- Continuing treatment until the storming episodes resolve, which may take days to weeks
It's also important to note that the use of beta blockers in patients with traumatic brain injury is not without risks, and the potential benefits must be weighed against the potential risks of hypotension and other adverse effects 1. However, the current evidence suggests that beta blockers can be a useful tool in managing neurostorming and improving outcomes in patients with traumatic brain injury.
From the FDA Drug Label
CLINICAL PHARMACOLOGY General Propranolol is a nonselective beta-adrenergic receptor blocking agent possessing no other autonomic nervous system activity. Mechanism of Action The effects of propranolol are due to selective blockade of beta-adrenergic receptors, leaving alpha-adrenergic responses intact.
The FDA drug label does not answer the question about the use of beta blockers for neurostorming.
From the Research
Beta Blockers for Neurostorming
- Beta blockers, such as propranolol, have been studied for their potential to reduce sympathetic storming in patients with traumatic brain injury (TBI) 2, 3.
- The use of propranolol has been shown to decrease catecholamine levels, improve hemodynamic parameters, and enhance Glasgow Coma Scale (GCS) scores in patients with TBI 2.
- Paroxysmal sympathetic hyperactivity (PSH) is a condition characterized by elevated sympathetic activity, which can occur in patients with acquired brain injuries, and beta blockers may be used to manage this condition 4, 3.
- Dexmedetomidine, a selective α2-adrenoceptor agonist, has also been investigated for its neuroprotective properties and potential to reduce sympathetic storming, although its primary use is for sedation and analgesia 5, 6.
- The evidence suggests that beta blockers, particularly propranolol, may be effective in reducing the length of stay and mortality rate in moderate-severe TBI patients with PSH, but further studies are needed to define the terms and conditions of their use 3.
Mechanisms and Effects
- The mechanisms underlying the neuroprotective effects of beta blockers and dexmedetomidine involve neurotransmitter regulation, inflammatory response, oxidative stress, apoptotic pathway, autophagy, mitochondrial function, and other cell signaling pathways 5, 6.
- Beta blockers, such as propranolol, can reduce sympathetic activity, decrease catecholamine levels, and improve hemodynamic parameters, which may contribute to their neuroprotective effects 2, 3.
- Dexmedetomidine has been shown to exert protective effects on multiple organs, including the brain, and may have potential as a novel neuroprotective agent for a wide range of neurological disorders 5, 6.