Abstract
Introduction
Traumatic brain injury (TBI) is often associated with reduced cerebral blood flow (CBF) and an increased inflammatory response, which contributes to secondary brain injury. Stellate ganglion block (SGB) has been shown to improve cerebral haemodynamics in patients without TBI.
Methods
Twenty patients with moderate to severe TBI participated in this prospective, single-centre interventional study. SGB was performed ipsilateral to the most severely affected hemisphere via an ultrasound-guided lateral approach at the level of C6 with the administration of 8 mL of 0.5% levobupivacaine. Changes in cerebral haemodynamics were assessed by evaluating blood flow velocity in the ipsilateral middle cerebral artery (MCA) using transcranial colour-coded duplex ultrasonography before and after SGB. Other methods used to evaluate cerebral haemodynamic changes included: (a) changes in basal cerebral artery diameter measured by CTA before and after SGB; (b) interhemispheric differences in cerebral blood flow (CBF), cerebral blood volume (CBV) and time to maximum (TMAX) measured by computerised perfusion tomography (CTP) after SGB. The effects on intracranial pressure (ICP) and the safety of the method were assessed by measuring cerebral perfusion pressure (CPP), ICP and brain tissue oxygenation by near-infrared spectroscopy (NIRS) before and after SGB. The effects of SGB on the sterile neuroinflammatory response and on neuronal and glial injury were assessed by measuring inflammatory and brain injury biomarkers (IL-6, neuron-specific enolase (NSE), protein S100B and glial fibrillary acidic protein (GFAP)) before SGB, at 12 hours and at 24 hours after SGB.
Results
SGB significantly reduced blood flow velocity in the MCA, increased the diameter of the large basal cerebral arteries and improved CBF and CBV in certain regions of the ipsilateral hemisphere. A significant decrease in the levels of brain injury biomarkers, including IL-6, S100B, NSE and GFAP, was observed within 24 hours after the procedure. Intracranial pressure decreased after SGB, while CPP and brain tissue oxygenation improved significantly. No adverse effects or complications were observed in any of the patients.
Conclusions
SGB modulates cerebral haemodynamics and lowers intracranial pressure in patients with moderate to severe TBI, suggesting its potential as a neuroprotective intervention. Although these results highlight the therapeutic potential of SGB, further randomised controlled trials are needed to determine the optimal application protocols and to evaluate the short- and long-term benefits of SGB in the treatment of patients with traumatic brain injury.
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