Could trigeminal nerve stimulation be a novel approach for managing neurogenic shock?

Dear Editor, Neurogenic shock is a distributive shock caused by the loss of sympathetic tone due to spinal cord injury or central nervous system dysfunction. This condition results in hypotension, bradycardia, and inadequate tissue perfusion (Padilla-Zambrano et al., 2017; Azeez et al., 2020; Florez-Perdomo et al., 2024). Estimating the natural incidence of neurogenic shock is challenging. Some studies report an incidence of up to 31% following high cervical spinal injuries (C1 to C5) and 24% for lower cervical injuries (C6 to C7). In comparison, neurogenic shock of cardiogenic origin, such as that observed in patients with subarachnoid hemorrhage and cerebral infarction, has been more thoroughly studied. Current management strategies include fluid resuscitation, vasopressors, and atropine, but these strategies are not always effective in addressing the underlying pathophysiology. Trigeminal nerve stimulation (TNS), as demonstrated in the study by Li et al. (2019), shows potential in modulating autonomic nervous system activity and improving hemodynamics, making it an attractive candidate for the treatment of neurogenic shock. Figure 1 illustrates the phys- iopathological events associated with TNS in the management of neurogenic shock.Figure 1: Illustration of the physiopathological events associated with trigeminal nerve stimulation in neurogenic shock.Regarding the pathophysiology of neurogenic shock, three mechanisms can lead to this condition. There is distributive shock caused by autonomic dysfunction, characterized by compromised sympathetic pathways and parasympathetic excitation, resulting in vasodilation and bradycardia. This mechanism is often observed in cases of traumatic spinal cord injury and conditions such as Guillain–Barré syndrome. Cardiogenic shock is typically observed in subarachnoid hemorrhage, where myocardial stunning occurs due to catecholamine release, or in cerebral infarction involving the right insula. Adrenal insufficiency and hypopituitarism can also cause neurogenic shock. Neurogenic shock associated with spinal cord injury develops during the primary injury phase. The initial mechanical trauma involves traction and compression forces. Direct compression of neural elements by osteoligamentous structures and their instability results in damage to both the central and peripheral nervous systems. Blood vessel injury, axonal disruption, and neuronal membrane rupture occur as a consequence. Microhemorrhages develop within minutes in the central gray matter, extending radially and axially over the next few hours. Within minutes of injury, inflammation occurs in the spinal cord, affecting the full diameter of the spinal canal at the injury site and leading to ischemia secondary to the inflammation. Subsequent disruption of blood flow autoregulation leads to neurogenic spinal shock, resulting in systemic hypotension that exacerbates ischemia and the progression of spinal cord injury. Hypotension and neurogenic shock following acute spinal cord injury are distributive processes resulting from the loss of peripheral vasoconstrictor tone in arterioles and blood pooling within the peripheral vasculature. If the injury is above C4, damage to the phrenic nerve may result in respiratory arrest. Injuries between C5 and T10 impair the function of respiratory muscles, leading to hypoxia, hypercapnia, and bronchial congestion. Cardiovascular complications primarily occur in injuries above T5, where damaged nerves cause bradycardia and vasoplegia, leading to hypotension. The potential role of TNS explores the fact that neurogenic shock is characterized by a loss of sympathetic tone due to spinal cord or central nervous system injury. TNS has been shown to restore the balance between sympathetic and parasympathetic activity, which could help counteract the profound hypotension and bradycardia observed in neurogenic shock (Tucker et al., 1987; McCulloch et al., 1999). The activation of endogenous pressor responses plays a pivotal role in managing neurogenic shock. Basic research has demonstrated that TNS activates mechanisms that increase circulating catecholamine levels and improve hemodynamics, both of which are crucial for maintaining blood pressure in neurogenic shock (Tucker et al., 1987; McCulloch et al., 1999). Additionally, research has shown that TNS can improve brain perfusion and organ oxygenation. TNS has been found to enhance brain perfusion and delay hemodynamic decompensation in hemorrhagic shock. These effects may translate to improved systemic perfusion in neurogenic shock, where reduced cardiac output and vascular tone impair oxygen delivery (Li et al., 2019). Finally, a reduction of systemic inflammation can be obtained, as inflammatory responses can exacerbate tissue injury in neurogenic shock. The anti-inflammatory effects of TNS could mitigate this secondary damage. We believe that TNS represents a promising technique that could offer a novel approach for managing neurogenic shock, opening new perspectives in both treatment and research. LRMS is an employee of AV Healthcare Innovators, LLC (Madison, WI, USA). Open access statement: This is an open access journal, and articles are distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.